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Efficacy of GelMA MAVP MPs in promoting nerve end interface self-resolution. ( A ) Schematic of the peripheral sciatic nerve ligation (p-SNL) model with four experimental groups (i.e., MAVP, VAN, vehicle, and control) ( B ) Immunofluorescence (IF) staining of p-VEGFR2 and YAP (indicating mechanotransduction signaling). ( C ) The positive area percentage of p-VEGFR2 (n = 6). ( D ) Percentage of YAP in nuclear/cytoplasm (n = 6). ( E ) IF staining of proliferation signal (Ki-67) and vessel signal (CD31) for p-SNL animal. ( F ) Quantification of Ki-67/CD31 co-localization area percentage (n = 6). ( G ) IF co-staining of Ki-67 and macrophage marker F4/80. ( H ) Quantification of Ki-67/F4/80 co-localization area percentage (n = 6). ( I ) IF staining of scar <t>marker</t> <t>α-SMA.</t> ( J ) Quantification <t>of</t> <t>α-SMA-positive</t> area percentage (n = 6). Mean values are shown and error bars represent ± s.d., as analyzed by one-way ANOVA followed by the Tukey-Kramer test in ( C , D , F , H and J ). Biological replicates were used for all experiments. ns, p > 0.05, ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.
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Therapeutic efficacy of SGM in a diabetic skin wound model. a ) Experiment procedure (Created in part with BioRender.com ). b ) Digital photography of wound healing progression in different groups. c ) Quantification of relative wound area over 14 days. (*; compared with the control group. # ; compared with the DFO group. & ; compared with the GM-DFO group.). d ) H&E staining of different groups on day 7 post-wounding. e ) IF staining for endothelial marker CD31 (red) and smooth muscle <t>marker</t> <t>α-SMA</t> (green) in different groups. f ) Quantification of wound length and number of blood vessel. g ) H&E <t>and</t> <t>Masson</t> staining of different groups on day 14. h ) Radar plot comparing group performance based on wound area and microvessel density. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
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Therapeutic efficacy of SGM in a diabetic skin wound model. a ) Experiment procedure (Created in part with BioRender.com ). b ) Digital photography of wound healing progression in different groups. c ) Quantification of relative wound area over 14 days. (*; compared with the control group. # ; compared with the DFO group. & ; compared with the GM-DFO group.). d ) H&E staining of different groups on day 7 post-wounding. e ) IF staining for endothelial marker CD31 (red) and smooth muscle <t>marker</t> <t>α-SMA</t> (green) in different groups. f ) Quantification of wound length and number of blood vessel. g ) H&E <t>and</t> <t>Masson</t> staining of different groups on day 14. h ) Radar plot comparing group performance based on wound area and microvessel density. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
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Therapeutic efficacy of SGM in a diabetic skin wound model. a ) Experiment procedure (Created in part with BioRender.com ). b ) Digital photography of wound healing progression in different groups. c ) Quantification of relative wound area over 14 days. (*; compared with the control group. # ; compared with the DFO group. & ; compared with the GM-DFO group.). d ) H&E staining of different groups on day 7 post-wounding. e ) IF staining for endothelial marker CD31 (red) and smooth muscle <t>marker</t> <t>α-SMA</t> (green) in different groups. f ) Quantification of wound length and number of blood vessel. g ) H&E <t>and</t> <t>Masson</t> staining of different groups on day 14. h ) Radar plot comparing group performance based on wound area and microvessel density. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
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Therapeutic efficacy of SGM in a diabetic skin wound model. a ) Experiment procedure (Created in part with BioRender.com ). b ) Digital photography of wound healing progression in different groups. c ) Quantification of relative wound area over 14 days. (*; compared with the control group. # ; compared with the DFO group. & ; compared with the GM-DFO group.). d ) H&E staining of different groups on day 7 post-wounding. e ) IF staining for endothelial marker CD31 (red) and smooth muscle <t>marker</t> <t>α-SMA</t> (green) in different groups. f ) Quantification of wound length and number of blood vessel. g ) H&E <t>and</t> <t>Masson</t> staining of different groups on day 14. h ) Radar plot comparing group performance based on wound area and microvessel density. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
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The expression of alpha-smooth muscle <t>actin</t> <t>(α-SMA)</t> protein. A) Immunostaining <t>of</t> <t>α-SMA.</t> (B): Quantification <t>of</t> <t>α-SMA</t> intensity expression in positive cells. Data are expressed as mean ± standard deviation (three separate experiments with three replicates in each). *P < 0.05. AA=ascorbic acid; Ang II=angiotensin II; Dex=dextran sulfate.
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The expression of alpha-smooth muscle <t>actin</t> <t>(α-SMA)</t> protein. A) Immunostaining <t>of</t> <t>α-SMA.</t> (B): Quantification <t>of</t> <t>α-SMA</t> intensity expression in positive cells. Data are expressed as mean ± standard deviation (three separate experiments with three replicates in each). *P < 0.05. AA=ascorbic acid; Ang II=angiotensin II; Dex=dextran sulfate.
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Efficacy of GelMA MAVP MPs in promoting nerve end interface self-resolution. ( A ) Schematic of the peripheral sciatic nerve ligation (p-SNL) model with four experimental groups (i.e., MAVP, VAN, vehicle, and control) ( B ) Immunofluorescence (IF) staining of p-VEGFR2 and YAP (indicating mechanotransduction signaling). ( C ) The positive area percentage of p-VEGFR2 (n = 6). ( D ) Percentage of YAP in nuclear/cytoplasm (n = 6). ( E ) IF staining of proliferation signal (Ki-67) and vessel signal (CD31) for p-SNL animal. ( F ) Quantification of Ki-67/CD31 co-localization area percentage (n = 6). ( G ) IF co-staining of Ki-67 and macrophage marker F4/80. ( H ) Quantification of Ki-67/F4/80 co-localization area percentage (n = 6). ( I ) IF staining of scar marker α-SMA. ( J ) Quantification of α-SMA-positive area percentage (n = 6). Mean values are shown and error bars represent ± s.d., as analyzed by one-way ANOVA followed by the Tukey-Kramer test in ( C , D , F , H and J ). Biological replicates were used for all experiments. ns, p > 0.05, ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Journal: Bioactive Materials

Article Title: Targeting VEGFR2 inhibition within a spatially-confined conduit promotes nerve self-resolution and alleviates mechanical allodynia

doi: 10.1016/j.bioactmat.2026.03.009

Figure Lengend Snippet: Efficacy of GelMA MAVP MPs in promoting nerve end interface self-resolution. ( A ) Schematic of the peripheral sciatic nerve ligation (p-SNL) model with four experimental groups (i.e., MAVP, VAN, vehicle, and control) ( B ) Immunofluorescence (IF) staining of p-VEGFR2 and YAP (indicating mechanotransduction signaling). ( C ) The positive area percentage of p-VEGFR2 (n = 6). ( D ) Percentage of YAP in nuclear/cytoplasm (n = 6). ( E ) IF staining of proliferation signal (Ki-67) and vessel signal (CD31) for p-SNL animal. ( F ) Quantification of Ki-67/CD31 co-localization area percentage (n = 6). ( G ) IF co-staining of Ki-67 and macrophage marker F4/80. ( H ) Quantification of Ki-67/F4/80 co-localization area percentage (n = 6). ( I ) IF staining of scar marker α-SMA. ( J ) Quantification of α-SMA-positive area percentage (n = 6). Mean values are shown and error bars represent ± s.d., as analyzed by one-way ANOVA followed by the Tukey-Kramer test in ( C , D , F , H and J ). Biological replicates were used for all experiments. ns, p > 0.05, ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Article Snippet: The following primary antibodies were used for the subsequent steps: anti-Yap (mouse, 1:200, Santa sc-376830); anti-p-VEGFR2 (rabbit, 1:100 Invitrogen, PA5-105765); α-SMA (rabbit, 1:200, Proteintech 14395-1-AP); Reca-1 (mouse, 1:200, Santa sc-52665); anti-CD31 (mouse, 1:200, Santa sc-13537); anti-Ki67 (rabbit, 1:150, Cell Signaling 9129S); anti-NF-200 (mouse, 1:200, Sigma, SAB4200747); anti-MBP (rabbit, 1:200, Abcam ab218011); anti-F4/80 (mouse, 1:200, Santa sc-377009); Iba-1 (rabbit, 1:150, Abcam ab178846); anti-CGRP (rabbit, 1:400, Abcam ab283568); anti-TRPA1 (mouse, 1:200, Santa sc-376495); anti-CD86 (rabbit, 1:200, Proteintech 30691-1-AP); CD206 (rabbit, 1:200, Proteintech 18704-1-AP).

Techniques: Ligation, Control, Immunofluorescence, Staining, Marker

Expression of pain signal proteins in peripheral nerve locations. ( A ) Immunohistochemical (IHC) imaging of VEGFA and ( B ) quantification of VEGFA mean integrated density (n = 6). ( C ) IHC staining for NGF and ( D ) quantification of NGF mean integrated density (n = 6). ( E ) IF staining for macrophages (F4/80) and ( F ) quantification of macrophage number per 10 4 μm 2 (n = 6). ( G ) IF staining for scar tissue (α-SMA) and ( H ) quantification of α-SMA -positive area percentage (n = 6). ( I ) IF staining for myelin sheath (MBP) and axon (NF200) and ( J ) quantification of myelin sheath to axon area ratio (n = 6). ( K ) IF staining for pain-related mediators CGRP and TRPA1 and ( L ) quantification of CGRP (n = 6), and ( M ) TRPA1 (n = 6). Mean values are shown and error bars represent ± s.d., as analyzed by one-way ANOVA followed by the Tukey-Kramer test in ( B , D , F , H , J , L and M ). Biological replicates were used for all experiments. ns, p > 0.05, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Journal: Bioactive Materials

Article Title: Targeting VEGFR2 inhibition within a spatially-confined conduit promotes nerve self-resolution and alleviates mechanical allodynia

doi: 10.1016/j.bioactmat.2026.03.009

Figure Lengend Snippet: Expression of pain signal proteins in peripheral nerve locations. ( A ) Immunohistochemical (IHC) imaging of VEGFA and ( B ) quantification of VEGFA mean integrated density (n = 6). ( C ) IHC staining for NGF and ( D ) quantification of NGF mean integrated density (n = 6). ( E ) IF staining for macrophages (F4/80) and ( F ) quantification of macrophage number per 10 4 μm 2 (n = 6). ( G ) IF staining for scar tissue (α-SMA) and ( H ) quantification of α-SMA -positive area percentage (n = 6). ( I ) IF staining for myelin sheath (MBP) and axon (NF200) and ( J ) quantification of myelin sheath to axon area ratio (n = 6). ( K ) IF staining for pain-related mediators CGRP and TRPA1 and ( L ) quantification of CGRP (n = 6), and ( M ) TRPA1 (n = 6). Mean values are shown and error bars represent ± s.d., as analyzed by one-way ANOVA followed by the Tukey-Kramer test in ( B , D , F , H , J , L and M ). Biological replicates were used for all experiments. ns, p > 0.05, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Article Snippet: The following primary antibodies were used for the subsequent steps: anti-Yap (mouse, 1:200, Santa sc-376830); anti-p-VEGFR2 (rabbit, 1:100 Invitrogen, PA5-105765); α-SMA (rabbit, 1:200, Proteintech 14395-1-AP); Reca-1 (mouse, 1:200, Santa sc-52665); anti-CD31 (mouse, 1:200, Santa sc-13537); anti-Ki67 (rabbit, 1:150, Cell Signaling 9129S); anti-NF-200 (mouse, 1:200, Sigma, SAB4200747); anti-MBP (rabbit, 1:200, Abcam ab218011); anti-F4/80 (mouse, 1:200, Santa sc-377009); Iba-1 (rabbit, 1:150, Abcam ab178846); anti-CGRP (rabbit, 1:400, Abcam ab283568); anti-TRPA1 (mouse, 1:200, Santa sc-376495); anti-CD86 (rabbit, 1:200, Proteintech 30691-1-AP); CD206 (rabbit, 1:200, Proteintech 18704-1-AP).

Techniques: Expressing, Immunohistochemical staining, Imaging, Immunohistochemistry, Staining

Therapeutic efficacy of SGM in a diabetic skin wound model. a ) Experiment procedure (Created in part with BioRender.com ). b ) Digital photography of wound healing progression in different groups. c ) Quantification of relative wound area over 14 days. (*; compared with the control group. # ; compared with the DFO group. & ; compared with the GM-DFO group.). d ) H&E staining of different groups on day 7 post-wounding. e ) IF staining for endothelial marker CD31 (red) and smooth muscle marker α-SMA (green) in different groups. f ) Quantification of wound length and number of blood vessel. g ) H&E and Masson staining of different groups on day 14. h ) Radar plot comparing group performance based on wound area and microvessel density. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Journal: Bioactive Materials

Article Title: A nature-derived, strong adhesive hydrogel microsphere for wet tissue repair: Multifunctional and clinical potential

doi: 10.1016/j.bioactmat.2026.01.033

Figure Lengend Snippet: Therapeutic efficacy of SGM in a diabetic skin wound model. a ) Experiment procedure (Created in part with BioRender.com ). b ) Digital photography of wound healing progression in different groups. c ) Quantification of relative wound area over 14 days. (*; compared with the control group. # ; compared with the DFO group. & ; compared with the GM-DFO group.). d ) H&E staining of different groups on day 7 post-wounding. e ) IF staining for endothelial marker CD31 (red) and smooth muscle marker α-SMA (green) in different groups. f ) Quantification of wound length and number of blood vessel. g ) H&E and Masson staining of different groups on day 14. h ) Radar plot comparing group performance based on wound area and microvessel density. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: The sample blocks were cut into 6 μm sections, followed by histological analysis with H&E and Masson trichromatic staining and immunofluorescence double staining with CD31 (Servicebio, China) and α-SMA (Servicebio, China), showing vascularization of the implanted structure.

Techniques: Drug discovery, Control, Staining, Marker

The expression of alpha-smooth muscle actin (α-SMA) protein. A) Immunostaining of α-SMA. (B): Quantification of α-SMA intensity expression in positive cells. Data are expressed as mean ± standard deviation (three separate experiments with three replicates in each). *P < 0.05. AA=ascorbic acid; Ang II=angiotensin II; Dex=dextran sulfate.

Journal: Brazilian Journal of Cardiovascular Surgery

Article Title: Optimization of the in vitro Model of Cardiac Fibrosis

doi: 10.21470/1678-9741-2025-0075

Figure Lengend Snippet: The expression of alpha-smooth muscle actin (α-SMA) protein. A) Immunostaining of α-SMA. (B): Quantification of α-SMA intensity expression in positive cells. Data are expressed as mean ± standard deviation (three separate experiments with three replicates in each). *P < 0.05. AA=ascorbic acid; Ang II=angiotensin II; Dex=dextran sulfate.

Article Snippet: Next, the cells were incubated with primary antibodies against α-SMA (mouse, Zytomed Systems) or vimentin (1:400, mouse, Sigma, Germany) 75 minutes at room temperature and overnight at 4°C, respectively.

Techniques: Expressing, Immunostaining, Standard Deviation