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Submission: On June 13 via api from US — Scanned from DE
Submission Tags: falconsandbox
Submission: On June 13 via api from US — Scanned from DE
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<a href="/1999-4923/15/9/2305/pdf?version=1694502578" class="UD_Listings_ArticlePDF" title="Article PDF" data-name="A Nucleus-Targeting WT1 Antagonistic Peptide Encapsulated in Polymeric Nanomicelles Combats Refractory Chronic Myeloid Leukemia" data-journal="pharmaceutics">
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data-editorschoiceaddition="<a href="/journal/pharmaceutics/editors_choice">More Editor’s choice articles in journal <em>Pharmaceutics</em>.</a>">Editor’s Choice</span><span class="label articletype">Article</span></div>
<a class="title-link" href="/1999-4923/15/9/2305">A Nucleus-Targeting WT1 Antagonistic Peptide Encapsulated in Polymeric Nanomicelles Combats Refractory Chronic Myeloid Leukemia</a>
<div class="authors"> by <span class="inlineblock "><strong>Mengting Chen</strong>, </span><span class="inlineblock "><strong>Xiaocui Fang</strong>, </span><span class="inlineblock "><strong>Rong Du</strong>, </span><span
class="inlineblock "><strong>Jie Meng</strong>, </span><span class="inlineblock "><strong>Jingyi Liu</strong>, </span><span class="inlineblock "><strong>Mingpeng Liu</strong>, </span><span class="inlineblock "><strong>Yanlian
Yang</strong> and </span><span class="inlineblock "><strong>Chen Wang</strong></span> </div>
<div class="color-grey-dark">
<em>Pharmaceutics</em> <b>2023</b>, <em>15</em>(9), 2305; <a href="https://doi.org/10.3390/pharmaceutics15092305">https://doi.org/10.3390/pharmaceutics15092305</a> - 12 Sep 2023
</div> Viewed by 1097 <div class="abstract-div">
<a href="#" onclick="$(this).next('.abstract-cropped').toggleClass('inline').next('.abstract-full').toggleClass('inline'); return false;">
<strong>Abstract </strong>
</a>
<div class="abstract-cropped inline"> Chronic myeloid leukemia (CML) is recognized as a classic clonal myeloproliferative disorder. Given the limited treatment options for CML patients in the accelerated phase (AP) and blast phase (BP),
there is an evident need to develop new therapeutic strategies. This has the potential
<a href="#" data-counterslink="https://www.mdpi.com/1999-4923/15/9/2305/more" onclick="$(this).parents('.abstract-cropped').toggleClass('inline').next('.abstract-full').toggleClass('inline'); return false;"> [...] Read more.</a>
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<div class="abstract-full "> Chronic myeloid leukemia (CML) is recognized as a classic clonal myeloproliferative disorder. Given the limited treatment options for CML patients in the accelerated phase (AP) and blast phase (BP), there is an
evident need to develop new therapeutic strategies. This has the potential to improve outcomes for individuals in the advanced stages of CML. A promising therapeutic target is Wilms’ tumor 1 (WT1), which is highly expressed in BP-CML
cells and plays a crucial role in CML progression. In this study, a chemically synthesized nucleus-targeting WT1 antagonistic peptide termed WIP2W was identified. The therapeutic implications of both the peptide and its micellar
formulation, M—WIP2W, were evaluated in WT1<sup>+</sup> BP-CML cell lines and in mice. The findings indicate that WIP2W can bind specifically to the WT1 protein, inducing cell cycle arrest and notable cytotoxicity in WT1<sup>+</sup>
BP-CML cells. Moreover, subcutaneous injections of M—WIP2W were observed to significantly enhance intra-tumoral accumulation and to effectively inhibit tumor growth. Thus, WIP2W stands out as a potent and selective WT1 inhibitor, and the
M—WIP2W nanoformulation appears promising for the therapeutic treatment of refractory CML as well as other WT1-overexpressing malignant cancers. <a href="/1999-4923/15/9/2305">Full article</a>
</div>
</div>
<div class="belongsTo" style="margin-bottom: 10px;"> (This article belongs to the Special Issue <a href="
/journal/pharmaceutics/special_issues/20B8UTBD00
">Functional Peptide-Based Biomaterials for Biomedical Applications</a>)<br>
</div>
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<strong>Figure 1</strong><br/>
<p>WIP2W could specifically bind to the WT1 protein overexpressed in K562 cells. (<b>A</b>) WT1 subcellular expression was evaluated via immunoblot analysis using an anti-WT1 antibody. (<b>B</b>) Intracellular localization of WT1 protein in K562 cells was examined via immunofluorescence assay. The blue fluorescence signifies the nucleus. The red signal represents the WT1 protein. The right figure displays the co-localization (scale bars: 20 μm). (<b>C</b>) Cellular uptake of FITC-WIP2W (0.05, 0.5, and 5 μM) by K562 cells was determined using flow cytometry after incubation at 37 °C for 2 h. Results from triplicate experiments were analyzed using GraphPad Prism 8. Data are presented as mean ± SD. (<b>D</b>) Schematic illustration of the pull-down assay. Created with BioRender.com. (<b>E</b>) Eluates obtained from the pull-downs (nucleus and cytoplasm protein) were subjected to Western blot assay using an anti-WT1 antibody. No WIP2W-modified magnetic beads were incubated with cell lysates and served as vehicle control. Cell lysate (5% input) served as a positive control.</p>
<strong style='display: block; margin-top: 10px; font-size: 18px;'><a style='color: #fff' href='/1999-4923/15/9/2305'>Full article</a></strong>
"></a><a href="https://pub.mdpi-res.com/pharmaceutics/pharmaceutics-15-02305/article_deploy/html/images/pharmaceutics-15-02305-g002-550.jpg?1694502653" title="
<strong>Figure 2</strong><br/>
<p>WIP2W effectively induced cell death and cycle arrest in K562 cells. (<b>A</b>) Cytotoxicity of WIP2W on different cell lines. K562 cells (1.5 × 10<sup>4</sup>/well) and L02 cells (8 × 10<sup>3</sup>/well) were exposed to different concentrations of WIP2W (1, 5, 10, 20, and 40 μM) for 24 h. PBS-treated K562 and L02 cells were used as controls (100%). Results are presented as mean ± SD (<span class="html-italic">n</span> = 6). The inserted graphic shows the WT1 expression levels of K562 and L02 cells. GAPDH served as the reference protein. (<b>B</b>) Cell cycle distribution of the K562 cells was determined using flow cytometry after treatment with 10 μM WIP2W for 24 h. Results are represented as mean ± SD (<span class="html-italic">n</span> = 3, *** <span class="html-italic">p</span> &lt; 0.001). (<b>C</b>) Representative flow cytometry images of cell cycle assay.</p>
<strong style='display: block; margin-top: 10px; font-size: 18px;'><a style='color: #fff' href='/1999-4923/15/9/2305'>Full article</a></strong>
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<strong>Figure 3</strong><br/>
<p>Gene expression changed in WIP2W-treated K562 cells. (<b>A</b>) Heatmap showing a hierarchical clustering of the differentially expressed genes in K562 cells after treatment with 10 μM WIP2W when compared to the untreated group (control). (<b>B</b>) Altered signaling pathway analysis of K562 cells after WIP2W treatment. (<b>C</b>) Selection of the potential genes in regulating WIP2W-induced K562 cell growth inhibition.</p>
<strong style='display: block; margin-top: 10px; font-size: 18px;'><a style='color: #fff' href='/1999-4923/15/9/2305'>Full article</a></strong>
"></a><a href="https://pub.mdpi-res.com/pharmaceutics/pharmaceutics-15-02305/article_deploy/html/images/pharmaceutics-15-02305-g004-550.jpg?1694502657" title="
<strong>Figure 4</strong><br/>
<p>Characterization of empty PEG-PE micelles and WIP2W-encapsulating PEG-PE micelles (M—WIP2W). Particle sizes and morphology of (<b>A</b>) empty micelle and (<b>B</b>) M—WIP2W. (<b>C</b>) Mean fluorescence intensities of K562 cells after treatments with FITC-WIP2W (5 μM) and M—WIP2W (PEG-PE: 15 μM, FITC-WIP2W: 5 μM) in a complete medium for 2 h at 37 °C were determined using flow cytometry. * <span class="html-italic">p</span> &lt; 0.05. (<b>D</b>) Cytotoxicity of WIP2W (1, 5, 10, and 20 μM) and M—WIP2W (WIP2W: 1, 5, 10, and 20 μM; PEG-PE: 3, 15, 30, and 60 μM) on K562 cells after 48 h of incubation at 37 °C, respectively.</p>
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<strong>Figure 5</strong><br/>
<p>In vivo biodistribution and therapeutic effect of WIP2W and M—WIP2W in WT1<sup>+</sup> BP-CML mice. (<b>A</b>) WIP2W distribution in the dissected tumors and major organs after treatment with FITC-WIP2W (30 mg/kg) and M—WIP2W (molar ratio of PEG-PE:FITC-WIP2W = 3:1) via IVIS spectrum, respectively. Tumor volumes (mm<sup>3</sup>) (<b>B</b>) and body weights (g) (<b>C</b>) of WT1<sup>+</sup> BP-CML mice after different treatments with PBS (control), imatinib, WIP2W, and M—WIP2W were calculated every other day, respectively. * <span class="html-italic">p</span> &lt; 0.05; *** <span class="html-italic">p</span> &lt; 0.001; ns: No significance. (<b>D</b>) The excised tumors of WT1<sup>+</sup> BP-CML mice after PBS, WIP2W, and M—WIP2W treatments, were stained with H&amp;E and an anti-WT1 antibody (scale bar: 100 μm), respectively. (<b>E</b>) Statistical analysis of WT1 expression levels by measuring mean InterDen of WT1-stained areas from (<b>D</b>). The control group was set as 100%. *** <span class="html-italic">p</span> &lt; 0.001; ns: No significance.</p>
<strong style='display: block; margin-top: 10px; font-size: 18px;'><a style='color: #fff' href='/1999-4923/15/9/2305'>Full article</a></strong>
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<strong>Figure 6</strong><br/>
<p>Biological safety and splenic infiltration evaluation of WIP2W, M—WIP2W, and imatinib. (<b>A</b>) Histological organ changes in WT1<sup>+</sup> BP-CML mice after treatments with PBS (control), imatinib, WIP2W, and M—WIP2W, respectively (scale bar: 100 μm). (<b>B</b>) Statistical results of Ki67 fluorescent staining of spleen tissues after various treatments were obtained by measuring the fluorescence intensity from <a href="#app1-pharmaceutics-15-02305" class="html-app">Figure S6</a>. The data are presented as mean ± SD (<span class="html-italic">n</span> = 3). * <span class="html-italic">p</span> &lt; 0.05; ** <span class="html-italic">p</span> &lt; 0.01; *** <span class="html-italic">p</span> &lt; 0.001; ns: No significance.</p>
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<a class="title-link" href="/1999-4923/15/8/2145">Enhanced Cartilage and Subchondral Bone Repair Using Carbon Nanotube-Doped Peptide Hydrogel–Polycaprolactone Composite Scaffolds</a>
<div class="authors"> by <span class="inlineblock "><strong>Jiayi Lv</strong>, </span><span class="inlineblock "><strong>Yilun Wu</strong>, </span><span class="inlineblock "><strong>Zhicheng Cao</strong>, </span><span
class="inlineblock "><strong>Xu Liu</strong>, </span><span class="inlineblock "><strong>Yuzhi Sun</strong>, </span><span class="inlineblock "><strong>Po Zhang</strong>, </span><span class="inlineblock "><strong>Xin Zhang</strong>,
</span><span class="inlineblock "><strong>Kexin Tang</strong>, </span><span class="inlineblock "><strong>Min Cheng</strong>, </span><span class="inlineblock "><strong>Qingqiang Yao</strong> and </span><span
class="inlineblock "><strong>Yishen Zhu</strong></span> </div>
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<em>Pharmaceutics</em> <b>2023</b>, <em>15</em>(8), 2145; <a href="https://doi.org/10.3390/pharmaceutics15082145">https://doi.org/10.3390/pharmaceutics15082145</a> - 15 Aug 2023
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<div class="abstract-cropped inline"> A carbon nanotube-doped octapeptide self-assembled hydrogel (FEK/C) and a hydrogel-based polycaprolactone PCL composite scaffold (FEK/C<sub>3</sub>-S) were developed for cartilage and subchondral bone
repair. The composite scaffold demonstrated modulated microstructure, mechanical properties, and conductivity by adjusting CNT concentration. In vitro evaluations showed
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<div class="abstract-full "> A carbon nanotube-doped octapeptide self-assembled hydrogel (FEK/C) and a hydrogel-based polycaprolactone PCL composite scaffold (FEK/C<sub>3</sub>-S) were developed for cartilage and subchondral bone repair.
The composite scaffold demonstrated modulated microstructure, mechanical properties, and conductivity by adjusting CNT concentration. In vitro evaluations showed enhanced cell proliferation, adhesion, and migration of articular cartilage
cells, osteoblasts, and bone marrow mesenchymal stem cells. The composite scaffold exhibited good biocompatibility, low haemolysis rate, and high protein absorption capacity. It also promoted osteogenesis and chondrogenesis, with
increased mineralization, alkaline phosphatase (ALP) activity, and glycosaminoglycan (GAG) secretion. The composite scaffold facilitated accelerated cartilage and subchondral bone regeneration in a rabbit knee joint defect model.
Histological analysis revealed improved cartilage tissue formation and increased subchondral bone density. Notably, the FEK/C<sub>3</sub>-S composite scaffold exhibited the most significant cartilage and subchondral bone formation. The
FEK/C<sub>3</sub>-S composite scaffold holds great promise for cartilage and subchondral bone repair. It offers enhanced mechanical support, conductivity, and bioactivity, leading to improved tissue regeneration. These findings contribute
to the advancement of regenerative strategies for challenging musculoskeletal tissue defects. <a href="/1999-4923/15/8/2145">Full article</a>
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<strong>Figure 1</strong><br/>
<p>Characterization of CNT-doped FEK peptide hydrogels. (<b>A</b>) Images of CNT solution after sonication and the formed FEK or FEK/C hydrogels; (<b>B</b>) SEM images, (<b>C</b>) TEM images, (<b>D</b>) Raman spectrum, D/G/2D represent the corresponding characteristic peaks, respectively; and (<b>E</b>) circular dichroism chromatogram spectra of FEK-based hydrogels containing different concentration of CNTs.</p>
<strong style='display: block; margin-top: 10px; font-size: 18px;'><a style='color: #fff' href='/1999-4923/15/8/2145'>Full article</a></strong>
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<strong>Figure 2</strong><br/>
<p>Mechanical properties of CNT-doped FEK peptide hydrogels. (<b>A</b>) The rheological modulus of hydrogels at pH 3 and 7; and (<b>B</b>) the complex viscosity with angular frequency at pH 3 and 7.</p>
<strong style='display: block; margin-top: 10px; font-size: 18px;'><a style='color: #fff' href='/1999-4923/15/8/2145'>Full article</a></strong>
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<strong>Figure 3</strong><br/>
<p>Characterization of FEK/C hydrogel–PCL composite scaffolds. (<b>A</b>) Photographs of PCL and hydrogel–PCL composite scaffolds; (<b>B</b>) SEM images of scaffolds, with typical areas of hydrogels infilled in the scaffold skeletons (in red frames) and on the PCL surfaces (in yellow frames) are shown below, respectively; (<b>C</b>) FTIR spectra and (<b>D</b>) conductivities of PCL and hydrogel–PCL composite scaffolds. The “****” above the column represents the statistical significance of this group compared to the PCL.</p>
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<strong>Figure 4</strong><br/>
<p>Effects of CNT-doped peptide hydrogel on the biocompatibility and degradation of composite scaffolds. (<b>A</b>) Contact angles of water on the surface of scaffolds; (<b>B</b>) Protein absorption on scaffolds from 4 to 72 h; (<b>C</b>) Haemolysis rate of rabbit red blood cells incubated with scaffolds for 5 h. The “****” represents the statistical significance compared to the Positive; (<b>D</b>) The degradation of scaffolds in simulated body fluids for 30 days, with typical areas of infilled hydrogels (in red frames) and PCL surfaces (in yellow frames) shown below, respectively. Negative: negative control that incubated with 0.9% NaCl; Positive: positive control that incubated with deionized water. The “**”and “***” at the right end of each line represents the statistical significance of this group compared to the PCL.</p>
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<strong>Figure 5</strong><br/>
<p>Effect of composite scaffolds on cellular biocompatibility. (<b>A</b>) The optical density values at 450 nm (OD<sub>450</sub>) of ACs, OBs, and BMSCs incubated with scaffolds for 1–5 days; (<b>B</b>) The OD<sub>450</sub> values of ACs adhere on scaffolds after co-culture for 2–8 h; (<b>C</b>) The in vitro migration rate of BMSCs cultured with scaffolds. The “ns” refers to no significant differences between groups. The “*/**/***/****” at the right end of each line represents the statistical significance of this group compared to the PCL.</p>
<strong style='display: block; margin-top: 10px; font-size: 18px;'><a style='color: #fff' href='/1999-4923/15/8/2145'>Full article</a></strong>
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<strong>Figure 6</strong><br/>
<p>Effects of composite scaffolds on osteogenesis and chondrogenesis in vitro. (<b>A</b>) Alizarin red staining of BMSCs cultured with scaffolds for 14 days and (<b>B</b>) ALP staining of BMSCs for 7- and 14-day cultures; (<b>C</b>) The histogram diagram of ALP positive areas; (<b>D</b>) Quantification analysis of GAG secretion in the supernatant of BMSCs cultured with scaffolds; (<b>E</b>) The images of AC spheres stained with alcian blue, with high magnification images shown in the second row. The “*/**/***/****” above the column represents the statistical significance of this group as compared to the PCL.</p>
<strong style='display: block; margin-top: 10px; font-size: 18px;'><a style='color: #fff' href='/1999-4923/15/8/2145'>Full article</a></strong>
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<strong>Figure 7</strong><br/>
<p>Effects of composite scaffolds on articular cartilage and subchondral bone defect repair in rabbits (<b>A</b>) Images of rabbit knee joints after articular defect and scaffold implant 8 weeks post-surgery; (<b>B</b>) Micro-CT images of repaired knee joint from coronal central plane (upper panel), transverse central plane (middle panel), and sagittal central plane (lower panel). The defect area is shown in a red circle (top view) or a red square (side view); (<b>C</b>) Bone mass density, (<b>D</b>) bone volume/tissue volume, and (<b>E</b>) trabeculae numbers calculated from Micro-CT. The “*/**” above the column represents the statistical significance of this group compared to the PCL.</p>
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<strong>Figure 8</strong><br/>
<p>Histological analysis of rabbit knee joints. (<b>A</b>) H and E staining of the knee joint (first row) with high magnification of the cartilage (second row) and subchondral bone (third row); (<b>B</b>) Safranin-O/fast green staining and (<b>C</b>) Masson staining of the defect joint after being treated with different scaffold for 8 weeks. Black and red arrows indicated cartilage and subchondral bone, respectively.</p>
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<strong>Scheme 1</strong><br/>
<p>Schematic illustration of the fabrication of CNT-doped peptide hydrogel–PCL composite scaffolds and their application in articular defect repair. Scale bars: 25 μm (white) and 1 mm (black).</p>
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<a href="/1999-4923/15/4/1272/pdf?version=1682559763" class="UD_Listings_ArticlePDF" title="Article PDF" data-name="Human Salivary Histatin-1 Attenuates Osteoarthritis through Promoting M1/M2 Macrophage Transition" data-journal="pharmaceutics">
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<a class="title-link" href="/1999-4923/15/4/1272">Human Salivary Histatin-1 Attenuates Osteoarthritis through Promoting M1/M2 Macrophage Transition</a>
<div class="authors"> by <span class="inlineblock "><strong>Antong Wu</strong>, </span><span class="inlineblock "><strong>Janak Lal. Pathak</strong>, </span><span class="inlineblock "><strong>Xingyang Li</strong>, </span><span
class="inlineblock "><strong>Wei Cao</strong>, </span><span class="inlineblock "><strong>Wenchao Zhong</strong>, </span><span class="inlineblock "><strong>Mingjing Zhu</strong>, </span><span class="inlineblock "><strong>Qiuyu Wu</strong>,
</span><span class="inlineblock "><strong>Wanyi Chen</strong>, </span><span class="inlineblock "><strong>Qiao Han</strong>, </span><span class="inlineblock "><strong>Siqing Jiang</strong>, </span><span class="inlineblock "><strong>Yuzhuo
Hei</strong>, </span><span class="inlineblock "><strong>Ziyi Zhang</strong>, </span><span class="inlineblock "><strong>Gang Wu</strong> and </span><span class="inlineblock "><strong>Qingbin Zhang</strong></span> </div>
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<em>Pharmaceutics</em> <b>2023</b>, <em>15</em>(4), 1272; <a href="https://doi.org/10.3390/pharmaceutics15041272">https://doi.org/10.3390/pharmaceutics15041272</a> - 18 Apr 2023
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<div class="abstract-cropped inline"> Osteoarthritis (OA) is an inflammation-driven degenerative joint disease. Human salivary peptide histatin-1 (Hst1) shows pro-healing and immunomodulatory properties. but its role in OA treatment is not
fully understood. In this study, we investigated the efficacy of Hst1 in the inflammation modulation-mediated attenuation of
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<div class="abstract-full "> Osteoarthritis (OA) is an inflammation-driven degenerative joint disease. Human salivary peptide histatin-1 (Hst1) shows pro-healing and immunomodulatory properties. but its role in OA treatment is not fully
understood. In this study, we investigated the efficacy of Hst1 in the inflammation modulation-mediated attenuation of bone and cartilage damage in OA. Hst1 was intra-articularly injected into a rat knee joint in a monosodium iodoacetate
(MIA)-induced OA model. Micro-CT, histological, and immunohistochemical analyses showed that Hst1 significantly attenuates cartilage and bone deconstruction as well as macrophage infiltration. In the lipopolysaccharide-induced air pouch
model, Hst1 significantly reduced inflammatory cell infiltration and inflammation. Enzyme-linked immunosorbent assay (ELISA), RT-qPCR, Western blot, immunofluorescence staining, flow cytometry (FCM), metabolic energy analysis, and
high-throughput gene sequencing showed that Hst1 significantly triggers M1-to-M2 macrophage phenotype switching, during which it significantly downregulated nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinases (MAPK)
signaling pathways. Furthermore, cell migration assay, Alcian blue, Safranin O staining, RT-qPCR, Western blot, and FCM showed that Hst1 not only attenuates M1-macrophage-CM-induced apoptosis and matrix metalloproteinase expression in
chondrogenic cells, but it also restores their metabolic activity, migration, and chondrogenic differentiation. These findings show the promising potential of Hst1 in treating OA. <a href="/1999-4923/15/4/1272">Full article</a>
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<div class="belongsTo" style="margin-bottom: 10px;"> (This article belongs to the Special Issue <a href="
/journal/pharmaceutics/special_issues/20B8UTBD00
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<strong>Figure 1</strong><br/>
<p>Hst1 attenuated bone and cartilage damage in MIA-induced knee OA. (<b>A</b>) The procedure of creating the rat knee OA model and administering Hst1 treatment. (<b>B</b>) Three-dimensional micro-CT images of the transverse section, coronal, and sagittal planes of the knee joint, scale bar = 1 mm. (<b>C</b>) Quantitative analysis of skeletal parameters BV, BV/TV, Tb. N, and Tb.Sp. (<b>D</b>) Knee joint tissue sections were stained with S&amp;F and H&amp;E, and OARSI was used for quantitative analysis, scale bar = 1 mm. (<b>E</b>) Representative images of Aggrecan immunohistochemical staining of knee joint tissue sections, scale bar = 40 μm. Data are expressed as means ± SD from three independent experiments. Significant differences compared to control group: ** <span class="html-italic">p</span> &lt; 0.01 and *** <span class="html-italic">p</span> &lt; 0.001, and compared to MIA group: # <span class="html-italic">p</span> &lt; 0.05 and ## <span class="html-italic">p</span> &lt; 0.01; ns: not significant.</p>
<strong style='display: block; margin-top: 10px; font-size: 18px;'><a style='color: #fff' href='/1999-4923/15/4/1272'>Full article</a></strong>
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<strong>Figure 2</strong><br/>
<p>Hst1 reduced macrophage infiltration in the MIA-induced knee OA. (<b>A</b>,<b>B</b>) Synovial macrophages of the knee joint were identified by using F4/80 immunohistochemistry; moreover, CD163 was chosen for marking M2 macrophages. (<b>C</b>,<b>D</b>) Quantitative analysis of synovial macrophages and M2 macrophages, scale bar = 40 μm. Data are expressed as means ± SD from three independent experiments. Significant differences compared to the control group: * <span class="html-italic">p</span> &lt; 0.05 and ** <span class="html-italic">p</span> &lt; 0.01, and compared to MIA group: # <span class="html-italic">p</span> &lt; 0.05.</p>
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<strong>Figure 3</strong><br/>
<p>Hst1 suppressed inflammation in acute air pouch model in mice. (<b>A</b>) The procedure of creating the mice air pouch model and administering Hst1 treatment. (<b>B</b>) The production levels of IL-6, IL-1β, and TNF-α in the air pouch lavage fluid were determined by using ELISA, n = 8. (<b>C</b>) H&amp;E staining of air pouch subcutaneous tissue sections, n = 3; scale bar = 200 μm in top row and 50 μm in bottom row. (<b>D</b>) Quantification of infiltrated cells and thickness of subcutaneous tissue, n = 3. Data are expressed as means ± SD from ≥ three independent experiments. Significant differences compared to control group: ** <span class="html-italic">p</span> &lt;0.01 and *** <span class="html-italic">p</span> &lt; 0.001, and compared to LPS group: # <span class="html-italic">p</span> &lt;0.05 and ### <span class="html-italic">p</span> &lt; 0.001; ns: not significant.</p>
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<strong>Figure 4</strong><br/>
<p>Hst1 promoted the M1-to-M2 macrophage phenotype transition. (<b>A</b>) CCK8 assay was used to analyze the metabolic activity of macrophages, n = 3. (<b>B</b>) Hst1-mediated mitigation of LPS-induced inflammatory cytokines IL-6, IL-1β, and TNF-α expression in macrophages determined by using ELISA, n = 3. (<b>C</b>) The production level of NO in LPS- and LPS+Hst1 (40 µM)-treated macrophages, n = 4. (<b>D</b>) mRNA level expressions of M1 macrophage markers IL-1β, IL-6, TNF-α, iNOS, and CD86 and of M2 macrophage markers IL-10, CD206, and Arg-1, n = 6. (<b>E</b>) Protein expressions of CD86 and CD206 in macrophages were analyzed by using Western blot, n = 3. Blots are cropped from <a href="#app1-pharmaceutics-15-01272" class="html-app">Supplementary File S1</a>. Data are expressed as means ± SD from ≥three independent experiments. Significant differences compared to the control group: *<span class="html-italic">p</span> &lt; 0.05, ** <span class="html-italic">p</span> &lt; 0.01, and *** <span class="html-italic">p</span> &lt; 0.001, and compared to LPS group: # <span class="html-italic">p</span> &lt; 0.05, ## <span class="html-italic">p</span> &lt; 0.01, and ###: <span class="html-italic">p</span> &lt; 0.001; ns: not significant.</p>
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<strong>Figure 5</strong><br/>
<p>Effects of Hst1 on the polarization phenotype of macrophages. (<b>A</b>) The M1 macrophage marker iNOS and M2 macrophage marker CD206 were incubated with primary antibody and observed using confocal microscopy, n = 3; scale bar = 50 μm. (<b>B</b>) M1 macrophage subsets evaluated using flow cytometry and by staining CD86, n = 3. (<b>C</b>) Energy metabolism of macrophages analyzed using seahorse analysis, n = 4. Data are expressed as means ± SD from ≥ three independent experiments. Significant differences compared to the control group: ** <span class="html-italic">p</span> &lt; 0.01, and *** <span class="html-italic">p</span> &lt; 0.001, and compared to LPS group: # <span class="html-italic">p</span> &lt; 0.05, ## <span class="html-italic">p</span> &lt;0.01, and ### <span class="html-italic">p</span> &lt; 0.001; ns: not significant.</p>
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<strong>Figure 6</strong><br/>
<p>High-throughput gene sequencing of macrophages. (<b>A</b>,<b>B</b>) Differential mRNA expression of RAW264.7 macrophages in each group. (<b>C</b>) mRNA intersections of LPS vs. control upregulated genes and LPS+Hst1 vs. LPS downregulated genes. Gene set enrichment analysis (GSEA) shows enrichment of the NF-κB and MAPK pathways. (<b>D</b>) Pathways positively enriched in LPS group vs. control group and (<b>E</b>) pathways negatively enriched in LPS+Hst1 group vs. LPS group.</p>
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<strong>Figure 7</strong><br/>
<p>Hst1 treatment downregulated NF-κB and MAPK signaling in LPS-treated macrophages. (<b>A</b>,<b>B</b>) Western blot analysis and qualification of NF-κB signaling-related proteins MAPK signaling-related proteins pERK/ERK, pJNK/JNK, and pP38/P38. Blots are cropped from <a href="#app1-pharmaceutics-15-01272" class="html-app">Supplementary File S2</a>. Data are expressed as means ± SD from three independent experiments. Significant differences compared to the control group: ** <span class="html-italic">p</span> &lt; 0.01 and *** <span class="html-italic">p</span> &lt; 0.001, and compared to LPS group: # <span class="html-italic">p</span> &lt; 0.05, ## <span class="html-italic">p</span> &lt; 0.01, and ### <span class="html-italic">p</span> &lt; 0.001.</p>
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<strong>Figure 8</strong><br/>
<p>CM from Hst1-treated macrophages promoted ATDC5 cells’ metabolic activity, migration, and differentiation. (<b>A</b>) CCK8 assay was used to detect the effect of macrophage CM on the metabolic activity of ATDC5 cells. (<b>B</b>) Transwell was used to observe ATDC5 cells migration, scale bar = 500 μm. (<b>C</b>,<b>D</b>) Safranin O and Alcian blue staining of ATDC5 cells cultured with macrophage CM for 7 days and quantification, scale bar = 500 μm. Data are expressed as mean ± SD from three independent experiments. Significant differences compared to the control-CM group: *<span class="html-italic">p</span> &lt; 0.05 and ***<span class="html-italic">p</span> &lt; 0.001, and compared to the LPS-CM group: #<span class="html-italic">p</span> &lt; 0.05, ##<span class="html-italic">p</span> &lt; 0.01, and ###<span class="html-italic">p</span> &lt; 0.001.</p>
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<strong>Figure 9</strong><br/>
<p>CM from Hst1-treated macrophages promoted ATDC5 cell differentiation and reduced chondrocyte destruction. (<b>A</b>) RT-qPCR results of chondrogenic differentiation markers Col-2, Sox-9, Aggrecan, and cartilage catabolism-related markers MMP-3, MMP-9, MMP-13, and Adamts5. (<b>B</b>) Western blot analysis and quantification of chondrogenic markers Col-2, Sox-9, and Aggrecan, and cartilage catabolism-related markers MMP-2, MMP-3, and MMP-9. (<b>C</b>) ATDC5 cells were cultured with macrophage CM for 7 days. Blots are cropped from <a href="#app1-pharmaceutics-15-01272" class="html-app">Supplementary File S3</a>. Data are expressed as means ± SD from three independent experiments. Significant differences compared to the control-CM group: ** <span class="html-italic">p</span> &lt; 0.01 and *** <span class="html-italic">p</span> &lt; 0.001, and compared to the LPS-CM group: # <span class="html-italic">p</span> &lt; 0.05, ## <span class="html-italic">p</span> &lt; 0.01, and ### <span class="html-italic">p</span> &lt; 0.001.</p>
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<strong>Figure 10</strong><br/>
<p>CM from Hst1-treated macrophages reduced ATDC5 cell apoptosis. (<b>A</b>) RT-qPCR analysis for apoptosis-related genes Bax and caspase-3. (<b>B-C</b>) The apoptosis rate of ATDC5 cells was analyzed using flow cytometry with annexin V-FITC/PI apoptosis analysis. (<b>D</b>) Western blot analysis and quantification of apoptosis-related proteins Bax, Bcl-2, and cleaved caspase-3. ATDC5 cells were cultured with macrophage CM for 7 days. Blots are cropped from <a href="#app1-pharmaceutics-15-01272" class="html-app">Supplementary File S4</a>. Data are expressed as means ± SD from three independent experiments. Significant differences compared to control-CM group: *** <span class="html-italic">p</span> &lt; 0.001, and compared to LPS-CM group: # <span class="html-italic">p</span> &lt; 0.05, ## <span class="html-italic">p</span> &lt; 0.01, and ### <span class="html-italic">p</span> &lt; 0.001.</p>
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<a class="title-link" href="/1999-4923/15/8/2093">Recent Advances of Cell-Penetrating Peptides and Their Application as Vectors for Delivery of Peptide and Protein-Based Cargo Molecules</a>
<div class="authors"> by <span class="inlineblock "><strong>Huifeng Zhang</strong>, </span><span class="inlineblock "><strong>Yanfei Zhang</strong>, </span><span class="inlineblock "><strong>Chuang Zhang</strong>, </span><span
class="inlineblock "><strong>Huan Yu</strong>, </span><span class="inlineblock "><strong>Yinghui Ma</strong>, </span><span class="inlineblock "><strong>Zhengqiang Li</strong> and </span><span class="inlineblock "><strong>Nianqiu
Shi</strong></span> </div>
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<em>Pharmaceutics</em> <b>2023</b>, <em>15</em>(8), 2093; <a href="https://doi.org/10.3390/pharmaceutics15082093">https://doi.org/10.3390/pharmaceutics15082093</a> - 7 Aug 2023
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<div class="abstract-cropped inline"> Peptides and proteins, two important classes of biomacromolecules, play important roles in the biopharmaceuticals field. As compared with traditional drugs based on small molecules, peptide- and
protein-based drugs offer several advantages, although most cannot traverse the cell membrane, a natural barrier that prevents
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<div class="abstract-full "> Peptides and proteins, two important classes of biomacromolecules, play important roles in the biopharmaceuticals field. As compared with traditional drugs based on small molecules, peptide- and protein-based
drugs offer several advantages, although most cannot traverse the cell membrane, a natural barrier that prevents biomacromolecules from directly entering cells. However, drug delivery via cell-penetrating peptides (CPPs) is increasingly
replacing traditional approaches that mediate biomacromolecular cellular uptake, due to CPPs’ superior safety and efficiency as drug delivery vehicles. In this review, we describe the discovery of CPPs, recent developments in CPP design,
and recent advances in CPP applications for enhanced cellular delivery of peptide- and protein-based drugs. First, we discuss the discovery of natural CPPs in snake, bee, and spider venom. Second, we describe several synthetic types of
CPPs, such as cyclic CPPs, glycosylated CPPs, and D-form CPPs. Finally, we summarize and discuss cell membrane permeability characteristics and therapeutic applications of different CPPs when used as vehicles to deliver peptides and
proteins to cells, as assessed using various preclinical disease models. Ultimately, this review provides an overview of recent advances in CPP development with relevance to applications related to the therapeutic delivery of
biomacromolecular drugs to alleviate diverse diseases. <a href="/1999-4923/15/8/2093">Full article</a>
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<div class="belongsTo" style="margin-bottom: 10px;"> (This article belongs to the Special Issue <a href="
/journal/pharmaceutics/special_issues/20B8UTBD00
">Functional Peptide-Based Biomaterials for Biomedical Applications</a>)<br>
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<div id="article-1212142-popup" class="popupgallery" style="display: inline; line-height: 200%"><a href="https://pub.mdpi-res.com/pharmaceutics/pharmaceutics-15-02093/article_deploy/html/images/pharmaceutics-15-02093-g001-550.jpg?1691406400" title="
<strong>Figure 1</strong><br/>
<p>Cyclic CPPs mentioned in this article.</p>
<strong style='display: block; margin-top: 10px; font-size: 18px;'><a style='color: #fff' href='/1999-4923/15/8/2093'>Full article</a></strong>
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<strong>Figure 2</strong><br/>
<p>Structures of the bicyclic peptide library, peptide 2 (hit #4), and peptide 7. Amino acid residues in peptide 7 are numbered from the N- to C-terminus. The CPP sequence is shown in red, while residues modified during optimization are shown in blue. B, β -alanine; CPP, cell-penetrating peptide; Hmb, hydroxylmethylbenzoyl; Pra, propargylglycine; Δ, L-2,3-diaminopropionic acid (Dap). Reprinted with permission from [<a href="#B60-pharmaceutics-15-02093" class="html-bibr">60</a>]. Copyright 2018 American Chemical Society.</p>
<strong style='display: block; margin-top: 10px; font-size: 18px;'><a style='color: #fff' href='/1999-4923/15/8/2093'>Full article</a></strong>
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<strong>Figure 3</strong><br/>
<p>Synthesis of trimer Tat constructs. Synthesis of tri-Tat A and tri-cTat A (<b>A</b>) and synthesis of tri-Tat B and tri-cTat B (<b>D</b>). In silico-generated ball-and-stick model of linear Tat A trimer (<b>B</b>). In silico-generated ball-and-stick model of cyclic Tat A trimer (<b>C</b>). In silico-generated ball-and-stick model of linear Tat B trimer (<b>E</b>). In silico-generated ball-and-stick model of cylicTat B trimer (<b>F</b>). Reproduced with permission from reference [<a href="#B63-pharmaceutics-15-02093" class="html-bibr">63</a>].</p>
<strong style='display: block; margin-top: 10px; font-size: 18px;'><a style='color: #fff' href='/1999-4923/15/8/2093'>Full article</a></strong>
"></a><a href="https://pub.mdpi-res.com/pharmaceutics/pharmaceutics-15-02093/article_deploy/html/images/pharmaceutics-15-02093-g004-550.jpg?1691406397" title="
<strong>Figure 4</strong><br/>
<p>Peptide structure and membrane transport. (<b>A</b>) The peptide segregated domains along an alpha-helical scaffold. (<b>B</b>) Linear peptide primary sequence and heptad-based wheel diagram for the helical conformation of the peptide. (<b>C</b>) Membrane translocation and cellular internalization are modulated by the glycan residue. Reproduced with permission from reference [<a href="#B70-pharmaceutics-15-02093" class="html-bibr">70</a>].</p>
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"></a><a href="https://pub.mdpi-res.com/pharmaceutics/pharmaceutics-15-02093/article_deploy/html/images/pharmaceutics-15-02093-g005-550.jpg?1691406398" title="
<strong>Figure 5</strong><br/>
<p>Applications of cell-penetrating peptides related to delivery of peptides and proteins into cells and across the epithelial barrier and blood–brain barrier (generated using Figdraw).</p>
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and Public Health</label></li>
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Medicine</label></li>
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<li class=""><label for="ms-opt-251" style="padding-left: 23px;"><input type="checkbox" value="jzbg" title="Journal of Zoological and Botanical Gardens" id="ms-opt-251">Journal of Zoological and Botanical Gardens</label></li>
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<li class=""><label for="ms-opt-254" style="padding-left: 23px;"><input type="checkbox" value="kinasesphosphatases" title="Kinases and Phosphatases" id="ms-opt-254">Kinases and Phosphatases</label></li>
<li class=""><label for="ms-opt-255" style="padding-left: 23px;"><input type="checkbox" value="knowledge" title="Knowledge" id="ms-opt-255">Knowledge</label></li>
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<li class=""><label for="ms-opt-317" style="padding-left: 23px;"><input type="checkbox" value="obesities" title="Obesities" id="ms-opt-317">Obesities</label></li>
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<li class=""><label for="ms-opt-319" style="padding-left: 23px;"><input type="checkbox" value="onco" title="Onco" id="ms-opt-319">Onco</label></li>
<li class=""><label for="ms-opt-320" style="padding-left: 23px;"><input type="checkbox" value="optics" title="Optics" id="ms-opt-320">Optics</label></li>
<li class=""><label for="ms-opt-321" style="padding-left: 23px;"><input type="checkbox" value="oral" title="Oral" id="ms-opt-321">Oral</label></li>
<li class=""><label for="ms-opt-322" style="padding-left: 23px;"><input type="checkbox" value="organics" title="Organics" id="ms-opt-322">Organics</label></li>
<li class=""><label for="ms-opt-323" style="padding-left: 23px;"><input type="checkbox" value="organoids" title="Organoids" id="ms-opt-323">Organoids</label></li>
<li class=""><label for="ms-opt-324" style="padding-left: 23px;"><input type="checkbox" value="osteology" title="Osteology" id="ms-opt-324">Osteology</label></li>
<li class=""><label for="ms-opt-325" style="padding-left: 23px;"><input type="checkbox" value="oxygen" title="Oxygen" id="ms-opt-325">Oxygen</label></li>
<li class=""><label for="ms-opt-326" style="padding-left: 23px;"><input type="checkbox" value="parasitologia" title="Parasitologia" id="ms-opt-326">Parasitologia</label></li>
<li class=""><label for="ms-opt-327" style="padding-left: 23px;"><input type="checkbox" value="particles" title="Particles" id="ms-opt-327">Particles</label></li>
<li class=""><label for="ms-opt-328" style="padding-left: 23px;"><input type="checkbox" value="pathogens" title="Pathogens" id="ms-opt-328">Pathogens</label></li>
<li class=""><label for="ms-opt-329" style="padding-left: 23px;"><input type="checkbox" value="pathophysiology" title="Pathophysiology" id="ms-opt-329">Pathophysiology</label></li>
<li class=""><label for="ms-opt-330" style="padding-left: 23px;"><input type="checkbox" value="pediatrrep" title="Pediatric Reports" id="ms-opt-330">Pediatric Reports</label></li>
<li class=""><label for="ms-opt-331" style="padding-left: 23px;"><input type="checkbox" value="pets" title="Pets" id="ms-opt-331">Pets</label></li>
<li class=""><label for="ms-opt-332" style="padding-left: 23px;"><input type="checkbox" value="pharmaceuticals" title="Pharmaceuticals" id="ms-opt-332">Pharmaceuticals</label></li>
<li class=""><label for="ms-opt-333" style="padding-left: 23px;"><input type="checkbox" value="pharmaceutics" title="Pharmaceutics" id="ms-opt-333">Pharmaceutics</label></li>
<li class=""><label for="ms-opt-334" style="padding-left: 23px;"><input type="checkbox" value="pharmacoepidemiology" title="Pharmacoepidemiology" id="ms-opt-334">Pharmacoepidemiology</label></li>
<li class=""><label for="ms-opt-335" style="padding-left: 23px;"><input type="checkbox" value="pharmacy" title="Pharmacy" id="ms-opt-335">Pharmacy</label></li>
<li class=""><label for="ms-opt-336" style="padding-left: 23px;"><input type="checkbox" value="philosophies" title="Philosophies" id="ms-opt-336">Philosophies</label></li>
<li class=""><label for="ms-opt-337" style="padding-left: 23px;"><input type="checkbox" value="photochem" title="Photochem" id="ms-opt-337">Photochem</label></li>
<li class=""><label for="ms-opt-338" style="padding-left: 23px;"><input type="checkbox" value="photonics" title="Photonics" id="ms-opt-338">Photonics</label></li>
<li class=""><label for="ms-opt-339" style="padding-left: 23px;"><input type="checkbox" value="phycology" title="Phycology" id="ms-opt-339">Phycology</label></li>
<li class=""><label for="ms-opt-340" style="padding-left: 23px;"><input type="checkbox" value="physchem" title="Physchem" id="ms-opt-340">Physchem</label></li>
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<li class=""><label for="ms-opt-345" style="padding-left: 23px;"><input type="checkbox" value="plasma" title="Plasma" id="ms-opt-345">Plasma</label></li>
<li class=""><label for="ms-opt-346" style="padding-left: 23px;"><input type="checkbox" value="platforms" title="Platforms" id="ms-opt-346">Platforms</label></li>
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<li class=""><label for="ms-opt-348" style="padding-left: 23px;"><input type="checkbox" value="polymers" title="Polymers" id="ms-opt-348">Polymers</label></li>
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<li class=""><label for="ms-opt-350" style="padding-left: 23px;"><input type="checkbox" value="poultry" title="Poultry" id="ms-opt-350">Poultry</label></li>
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<li class=""><label for="ms-opt-352" style="padding-left: 23px;"><input type="checkbox" value="proceedings" title="Proceedings" id="ms-opt-352">Proceedings</label></li>
<li class=""><label for="ms-opt-353" style="padding-left: 23px;"><input type="checkbox" value="processes" title="Processes" id="ms-opt-353">Processes</label></li>
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<li class=""><label for="ms-opt-355" style="padding-left: 23px;"><input type="checkbox" value="proteomes" title="Proteomes" id="ms-opt-355">Proteomes</label></li>
<li class=""><label for="ms-opt-356" style="padding-left: 23px;"><input type="checkbox" value="psychiatryint" title="Psychiatry International" id="ms-opt-356">Psychiatry International</label></li>
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<li class=""><label for="ms-opt-358" style="padding-left: 23px;"><input type="checkbox" value="psycholint" title="Psychology International" id="ms-opt-358">Psychology International</label></li>
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<li class=""><label for="ms-opt-361" style="padding-left: 23px;"><input type="checkbox" value="quantumrep" title="Quantum Reports" id="ms-opt-361">Quantum Reports</label></li>
<li class=""><label for="ms-opt-362" style="padding-left: 23px;"><input type="checkbox" value="quaternary" title="Quaternary" id="ms-opt-362">Quaternary</label></li>
<li class=""><label for="ms-opt-363" style="padding-left: 23px;"><input type="checkbox" value="radiation" title="Radiation" id="ms-opt-363">Radiation</label></li>
<li class=""><label for="ms-opt-364" style="padding-left: 23px;"><input type="checkbox" value="reactions" title="Reactions" id="ms-opt-364">Reactions</label></li>
<li class=""><label for="ms-opt-365" style="padding-left: 23px;"><input type="checkbox" value="realestate" title="Real Estate" id="ms-opt-365">Real Estate</label></li>
<li class=""><label for="ms-opt-366" style="padding-left: 23px;"><input type="checkbox" value="receptors" title="Receptors" id="ms-opt-366">Receptors</label></li>
<li class=""><label for="ms-opt-367" style="padding-left: 23px;"><input type="checkbox" value="recycling" title="Recycling" id="ms-opt-367">Recycling</label></li>
<li class=""><label for="ms-opt-368" style="padding-left: 23px;"><input type="checkbox" value="religions" title="Religions" id="ms-opt-368">Religions</label></li>
<li class=""><label for="ms-opt-369" style="padding-left: 23px;"><input type="checkbox" value="remotesensing" title="Remote Sensing" id="ms-opt-369">Remote Sensing</label></li>
<li class=""><label for="ms-opt-370" style="padding-left: 23px;"><input type="checkbox" value="reports" title="Reports" id="ms-opt-370">Reports</label></li>
<li class=""><label for="ms-opt-371" style="padding-left: 23px;"><input type="checkbox" value="reprodmed" title="Reproductive Medicine" id="ms-opt-371">Reproductive Medicine</label></li>
<li class=""><label for="ms-opt-372" style="padding-left: 23px;"><input type="checkbox" value="resources" title="Resources" id="ms-opt-372">Resources</label></li>
<li class=""><label for="ms-opt-373" style="padding-left: 23px;"><input type="checkbox" value="rheumato" title="Rheumato" id="ms-opt-373">Rheumato</label></li>
<li class=""><label for="ms-opt-374" style="padding-left: 23px;"><input type="checkbox" value="risks" title="Risks" id="ms-opt-374">Risks</label></li>
<li class=""><label for="ms-opt-375" style="padding-left: 23px;"><input type="checkbox" value="robotics" title="Robotics" id="ms-opt-375">Robotics</label></li>
<li class=""><label for="ms-opt-376" style="padding-left: 23px;"><input type="checkbox" value="ruminants" title="Ruminants" id="ms-opt-376">Ruminants</label></li>
<li class=""><label for="ms-opt-377" style="padding-left: 23px;"><input type="checkbox" value="safety" title="Safety" id="ms-opt-377">Safety</label></li>
<li class=""><label for="ms-opt-378" style="padding-left: 23px;"><input type="checkbox" value="sci" title="Sci" id="ms-opt-378">Sci</label></li>
<li class=""><label for="ms-opt-379" style="padding-left: 23px;"><input type="checkbox" value="scipharm" title="Scientia Pharmaceutica" id="ms-opt-379">Scientia Pharmaceutica</label></li>
<li class=""><label for="ms-opt-380" style="padding-left: 23px;"><input type="checkbox" value="sclerosis" title="Sclerosis" id="ms-opt-380">Sclerosis</label></li>
<li class=""><label for="ms-opt-381" style="padding-left: 23px;"><input type="checkbox" value="seeds" title="Seeds" id="ms-opt-381">Seeds</label></li>
<li class=""><label for="ms-opt-382" style="padding-left: 23px;"><input type="checkbox" value="sensors" title="Sensors" id="ms-opt-382">Sensors</label></li>
<li class=""><label for="ms-opt-383" style="padding-left: 23px;"><input type="checkbox" value="separations" title="Separations" id="ms-opt-383">Separations</label></li>
<li class=""><label for="ms-opt-384" style="padding-left: 23px;"><input type="checkbox" value="sexes" title="Sexes" id="ms-opt-384">Sexes</label></li>
<li class=""><label for="ms-opt-385" style="padding-left: 23px;"><input type="checkbox" value="signals" title="Signals" id="ms-opt-385">Signals</label></li>
<li class=""><label for="ms-opt-386" style="padding-left: 23px;"><input type="checkbox" value="sinusitis" title="Sinusitis" id="ms-opt-386">Sinusitis</label></li>
<li class=""><label for="ms-opt-387" style="padding-left: 23px;"><input type="checkbox" value="smartcities" title="Smart Cities" id="ms-opt-387">Smart Cities</label></li>
<li class=""><label for="ms-opt-388" style="padding-left: 23px;"><input type="checkbox" value="socsci" title="Social Sciences" id="ms-opt-388">Social Sciences</label></li>
<li class=""><label for="ms-opt-389" style="padding-left: 23px;"><input type="checkbox" value="siuj" title="Société Internationale d’Urologie Journal" id="ms-opt-389">Société Internationale d’Urologie Journal</label></li>
<li class=""><label for="ms-opt-390" style="padding-left: 23px;"><input type="checkbox" value="societies" title="Societies" id="ms-opt-390">Societies</label></li>
<li class=""><label for="ms-opt-391" style="padding-left: 23px;"><input type="checkbox" value="software" title="Software" id="ms-opt-391">Software</label></li>
<li class=""><label for="ms-opt-392" style="padding-left: 23px;"><input type="checkbox" value="soilsystems" title="Soil Systems" id="ms-opt-392">Soil Systems</label></li>
<li class=""><label for="ms-opt-393" style="padding-left: 23px;"><input type="checkbox" value="solar" title="Solar" id="ms-opt-393">Solar</label></li>
<li class=""><label for="ms-opt-394" style="padding-left: 23px;"><input type="checkbox" value="solids" title="Solids" id="ms-opt-394">Solids</label></li>
<li class=""><label for="ms-opt-395" style="padding-left: 23px;"><input type="checkbox" value="spectroscj" title="Spectroscopy Journal" id="ms-opt-395">Spectroscopy Journal</label></li>
<li class=""><label for="ms-opt-396" style="padding-left: 23px;"><input type="checkbox" value="sports" title="Sports" id="ms-opt-396">Sports</label></li>
<li class=""><label for="ms-opt-397" style="padding-left: 23px;"><input type="checkbox" value="standards" title="Standards" id="ms-opt-397">Standards</label></li>
<li class=""><label for="ms-opt-398" style="padding-left: 23px;"><input type="checkbox" value="stats" title="Stats" id="ms-opt-398">Stats</label></li>
<li class=""><label for="ms-opt-399" style="padding-left: 23px;"><input type="checkbox" value="stresses" title="Stresses" id="ms-opt-399">Stresses</label></li>
<li class=""><label for="ms-opt-400" style="padding-left: 23px;"><input type="checkbox" value="surfaces" title="Surfaces" id="ms-opt-400">Surfaces</label></li>
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FUNCTIONAL PEPTIDE-BASED BIOMATERIALS FOR BIOMEDICAL APPLICATIONS
* Special Issue Editors
* Special Issue Information
* Keywords
* Published Papers
A special issue of Pharmaceutics (ISSN 1999-4923). This special issue belongs to
the section "Biopharmaceutics".
Deadline for manuscript submissions: 30 June 2024 | Viewed by 7364
SHARE THIS SPECIAL ISSUE
SPECIAL ISSUE EDITORS
Prof. Dr. Yishen Zhu
Prof. Dr. Yishen Zhu
Scilit Preprints.org Google Scholar
E-Mail Website
Guest Editor
Pharmaceutical Engineering Department, Nanjing Technology University, Nanjing
210028, China
Interests: pharmaceutical technology, with emphasis in manufacturing processes
and dosage form design
Special Issues, Collections and Topics in MDPI journals
Special Issue in Pharmaceutics: Lipid-Based Dosage Form
Dr. Qingqiang Yao
Dr. Qingqiang Yao
Scilit Preprints.org Google Scholar
E-Mail Website
Guest Editor
Department of orthopaedic, Nanjing Medical University, Nanjing 210029, China
Interests: tissue engineering; materials engineering
SPECIAL ISSUE INFORMATION
Dear Colleagues,
Functional peptide-based biomaterials have been widely used in biomedical
application research, including peptides that can respond to different stimuli
(such as pH, redox potential, temperature, light and enzyme), self-assembly
peptide hydrogels, cell penetrating peptides, affinity peptides that interact
with receptors, and peptide-drug conjugates. Therefore, the intelligent and
multifunctional peptide based structural system can respond to environmental
stimuli, promote tissue repair and regeneration through the biomimetic
extracellular matrix structure, penetrate cell membranes, induce functional
effects by binding receptors, and deliver drug molecules in a single molecule,
which play an important role in the research of biomedical applications. The
purpose of this Special Issue of Pharmaceutics is to collect research and review
papers on biomedical applications of functional peptide-based biomaterials. We
welcome articles dealing with various aspects of functional peptide-based
biomaterials, and invite researchers and drug developers to publish their
original research or review articles, including expert opinions and perspectives
in the field of biomedical applications. The topics include but are not limited
to:
* Self-assembly peptide hydrogels for cell repair and regeneration;
* Environmental stimuli-responsive peptide-based biomaterials;
* Peptide drug delivery system;
* Cell penetrating peptides;
* Receptor-affinity peptides and the combinations;
* Peptide-drug conjugates in biomedical applications.
Prof. Dr. Yishen Zhu
Dr. Qingqiang Yao
Guest Editors
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publication or during author revisions.
KEYWORDS
* functional peptides
* biomedical applications
* tissue engineering
* environmental stimuli-responsive
* self-assembly peptide hydrogels
* affinity peptides
* peptide drug delivery system
* cell penetrating peptides
PUBLISHED PAPERS (4 PAPERS)
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RESEARCH
Jump to: Review
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Supplementary material:
Supplementary File 1 (ZIP, 610 KiB)
17 pages, 3726 KiB
Open AccessEditor’s ChoiceArticle
A Nucleus-Targeting WT1 Antagonistic Peptide Encapsulated in Polymeric
Nanomicelles Combats Refractory Chronic Myeloid Leukemia
by Mengting Chen, Xiaocui Fang, Rong Du, Jie Meng, Jingyi Liu, Mingpeng Liu,
Yanlian Yang and Chen Wang
Pharmaceutics 2023, 15(9), 2305; https://doi.org/10.3390/pharmaceutics15092305 -
12 Sep 2023
Viewed by 1097
Abstract
Chronic myeloid leukemia (CML) is recognized as a classic clonal
myeloproliferative disorder. Given the limited treatment options for CML
patients in the accelerated phase (AP) and blast phase (BP), there is an evident
need to develop new therapeutic strategies. This has the potential [...] Read
more.
Chronic myeloid leukemia (CML) is recognized as a classic clonal
myeloproliferative disorder. Given the limited treatment options for CML
patients in the accelerated phase (AP) and blast phase (BP), there is an evident
need to develop new therapeutic strategies. This has the potential to improve
outcomes for individuals in the advanced stages of CML. A promising therapeutic
target is Wilms’ tumor 1 (WT1), which is highly expressed in BP-CML cells and
plays a crucial role in CML progression. In this study, a chemically synthesized
nucleus-targeting WT1 antagonistic peptide termed WIP2W was identified. The
therapeutic implications of both the peptide and its micellar formulation,
M—WIP2W, were evaluated in WT1+ BP-CML cell lines and in mice. The findings
indicate that WIP2W can bind specifically to the WT1 protein, inducing cell
cycle arrest and notable cytotoxicity in WT1+ BP-CML cells. Moreover,
subcutaneous injections of M—WIP2W were observed to significantly enhance
intra-tumoral accumulation and to effectively inhibit tumor growth. Thus, WIP2W
stands out as a potent and selective WT1 inhibitor, and the M—WIP2W
nanoformulation appears promising for the therapeutic treatment of refractory
CML as well as other WT1-overexpressing malignant cancers. Full article
(This article belongs to the Special Issue Functional Peptide-Based Biomaterials
for Biomedical Applications)
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Supplementary File 1 (ZIP, 4338 KiB)
20 pages, 11414 KiB
Open AccessArticle
Enhanced Cartilage and Subchondral Bone Repair Using Carbon Nanotube-Doped
Peptide Hydrogel–Polycaprolactone Composite Scaffolds
by Jiayi Lv, Yilun Wu, Zhicheng Cao, Xu Liu, Yuzhi Sun, Po Zhang, Xin Zhang,
Kexin Tang, Min Cheng, Qingqiang Yao and Yishen Zhu
Pharmaceutics 2023, 15(8), 2145; https://doi.org/10.3390/pharmaceutics15082145 -
15 Aug 2023
Cited by 1 | Viewed by 1362
Abstract
A carbon nanotube-doped octapeptide self-assembled hydrogel (FEK/C) and a
hydrogel-based polycaprolactone PCL composite scaffold (FEK/C3-S) were developed
for cartilage and subchondral bone repair. The composite scaffold demonstrated
modulated microstructure, mechanical properties, and conductivity by adjusting
CNT concentration. In vitro evaluations showed [...] Read more.
A carbon nanotube-doped octapeptide self-assembled hydrogel (FEK/C) and a
hydrogel-based polycaprolactone PCL composite scaffold (FEK/C3-S) were developed
for cartilage and subchondral bone repair. The composite scaffold demonstrated
modulated microstructure, mechanical properties, and conductivity by adjusting
CNT concentration. In vitro evaluations showed enhanced cell proliferation,
adhesion, and migration of articular cartilage cells, osteoblasts, and bone
marrow mesenchymal stem cells. The composite scaffold exhibited good
biocompatibility, low haemolysis rate, and high protein absorption capacity. It
also promoted osteogenesis and chondrogenesis, with increased mineralization,
alkaline phosphatase (ALP) activity, and glycosaminoglycan (GAG) secretion. The
composite scaffold facilitated accelerated cartilage and subchondral bone
regeneration in a rabbit knee joint defect model. Histological analysis revealed
improved cartilage tissue formation and increased subchondral bone density.
Notably, the FEK/C3-S composite scaffold exhibited the most significant
cartilage and subchondral bone formation. The FEK/C3-S composite scaffold holds
great promise for cartilage and subchondral bone repair. It offers enhanced
mechanical support, conductivity, and bioactivity, leading to improved tissue
regeneration. These findings contribute to the advancement of regenerative
strategies for challenging musculoskeletal tissue defects. Full article
(This article belongs to the Special Issue Functional Peptide-Based Biomaterials
for Biomedical Applications)
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Supplementary File 1 (ZIP, 503 KiB)
22 pages, 9495 KiB
Open AccessArticle
Human Salivary Histatin-1 Attenuates Osteoarthritis through Promoting M1/M2
Macrophage Transition
by Antong Wu, Janak Lal. Pathak, Xingyang Li, Wei Cao, Wenchao Zhong, Mingjing
Zhu, Qiuyu Wu, Wanyi Chen, Qiao Han, Siqing Jiang, Yuzhuo Hei, Ziyi Zhang, Gang
Wu and Qingbin Zhang
Pharmaceutics 2023, 15(4), 1272; https://doi.org/10.3390/pharmaceutics15041272 -
18 Apr 2023
Cited by 3 | Viewed by 1600
Abstract
Osteoarthritis (OA) is an inflammation-driven degenerative joint disease. Human
salivary peptide histatin-1 (Hst1) shows pro-healing and immunomodulatory
properties. but its role in OA treatment is not fully understood. In this study,
we investigated the efficacy of Hst1 in the inflammation modulation-mediated
attenuation of [...] Read more.
Osteoarthritis (OA) is an inflammation-driven degenerative joint disease. Human
salivary peptide histatin-1 (Hst1) shows pro-healing and immunomodulatory
properties. but its role in OA treatment is not fully understood. In this study,
we investigated the efficacy of Hst1 in the inflammation modulation-mediated
attenuation of bone and cartilage damage in OA. Hst1 was intra-articularly
injected into a rat knee joint in a monosodium iodoacetate (MIA)-induced OA
model. Micro-CT, histological, and immunohistochemical analyses showed that Hst1
significantly attenuates cartilage and bone deconstruction as well as macrophage
infiltration. In the lipopolysaccharide-induced air pouch model, Hst1
significantly reduced inflammatory cell infiltration and inflammation.
Enzyme-linked immunosorbent assay (ELISA), RT-qPCR, Western blot,
immunofluorescence staining, flow cytometry (FCM), metabolic energy analysis,
and high-throughput gene sequencing showed that Hst1 significantly triggers
M1-to-M2 macrophage phenotype switching, during which it significantly
downregulated nuclear factor kappa-B (NF-κB) and mitogen-activated protein
kinases (MAPK) signaling pathways. Furthermore, cell migration assay, Alcian
blue, Safranin O staining, RT-qPCR, Western blot, and FCM showed that Hst1 not
only attenuates M1-macrophage-CM-induced apoptosis and matrix metalloproteinase
expression in chondrogenic cells, but it also restores their metabolic activity,
migration, and chondrogenic differentiation. These findings show the promising
potential of Hst1 in treating OA. Full article
(This article belongs to the Special Issue Functional Peptide-Based Biomaterials
for Biomedical Applications)
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REVIEW
Jump to: Research
30 pages, 3004 KiB
Open AccessReview
Recent Advances of Cell-Penetrating Peptides and Their Application as Vectors
for Delivery of Peptide and Protein-Based Cargo Molecules
by Huifeng Zhang, Yanfei Zhang, Chuang Zhang, Huan Yu, Yinghui Ma, Zhengqiang Li
and Nianqiu Shi
Pharmaceutics 2023, 15(8), 2093; https://doi.org/10.3390/pharmaceutics15082093 -
7 Aug 2023
Cited by 4 | Viewed by 2563
Abstract
Peptides and proteins, two important classes of biomacromolecules, play
important roles in the biopharmaceuticals field. As compared with traditional
drugs based on small molecules, peptide- and protein-based drugs offer several
advantages, although most cannot traverse the cell membrane, a natural barrier
that prevents [...] Read more.
Peptides and proteins, two important classes of biomacromolecules, play
important roles in the biopharmaceuticals field. As compared with traditional
drugs based on small molecules, peptide- and protein-based drugs offer several
advantages, although most cannot traverse the cell membrane, a natural barrier
that prevents biomacromolecules from directly entering cells. However, drug
delivery via cell-penetrating peptides (CPPs) is increasingly replacing
traditional approaches that mediate biomacromolecular cellular uptake, due to
CPPs’ superior safety and efficiency as drug delivery vehicles. In this review,
we describe the discovery of CPPs, recent developments in CPP design, and recent
advances in CPP applications for enhanced cellular delivery of peptide- and
protein-based drugs. First, we discuss the discovery of natural CPPs in snake,
bee, and spider venom. Second, we describe several synthetic types of CPPs, such
as cyclic CPPs, glycosylated CPPs, and D-form CPPs. Finally, we summarize and
discuss cell membrane permeability characteristics and therapeutic applications
of different CPPs when used as vehicles to deliver peptides and proteins to
cells, as assessed using various preclinical disease models. Ultimately, this
review provides an overview of recent advances in CPP development with relevance
to applications related to the therapeutic delivery of biomacromolecular drugs
to alleviate diverse diseases. Full article
(This article belongs to the Special Issue Functional Peptide-Based Biomaterials
for Biomedical Applications)
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