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mouse anti α sma  (R&D Systems)


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    Structured Review

    R&D Systems mouse anti α sma
    Mouse Anti α Sma, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 215 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/%CE%B1+smooth+muscle+actin/pmc13115125-76-10-14?v=R%26D+Systems
    Average 95 stars, based on 215 article reviews
    mouse anti α sma - by Bioz Stars, 2026-07
    95/100 stars

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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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    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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    In vivo angiogenic effects of HCH gel. (A) H&E staining of tissue sections showing the angiogenic effect after 4 weeks of hydrogel implantation. (B) Immunofluorescence co-staining for CD31 and <t>α-SMA</t> assessing vascular proliferation at 2 weeks post-implantation (scale bars = 200 μm). White dotted lines indicate the hydrogel–tissue interface. (C) Quantification of the CD31 + and α-SMA + area from graph B. (D) Immunofluorescence co-staining for CD31 and α-SMA at 4 weeks post-implantation (scale bars = 200 μm). (E) Quantification of the CD31 + and α-SMA + area from graph D. (n = 6, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001).
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    Servicebio Inc α smooth muscle actin αsma primary antibody
    In vivo angiogenic effects of HCH gel. (A) H&E staining of tissue sections showing the angiogenic effect after 4 weeks of hydrogel implantation. (B) Immunofluorescence co-staining for CD31 and <t>α-SMA</t> assessing vascular proliferation at 2 weeks post-implantation (scale bars = 200 μm). White dotted lines indicate the hydrogel–tissue interface. (C) Quantification of the CD31 + and α-SMA + area from graph B. (D) Immunofluorescence co-staining for CD31 and α-SMA at 4 weeks post-implantation (scale bars = 200 μm). (E) Quantification of the CD31 + and α-SMA + area from graph D. (n = 6, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001).
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    In vivo angiogenic effects of HCH gel. (A) H&E staining of tissue sections showing the angiogenic effect after 4 weeks of hydrogel implantation. (B) Immunofluorescence co-staining for CD31 and <t>α-SMA</t> assessing vascular proliferation at 2 weeks post-implantation (scale bars = 200 μm). White dotted lines indicate the hydrogel–tissue interface. (C) Quantification of the CD31 + and α-SMA + area from graph B. (D) Immunofluorescence co-staining for CD31 and α-SMA at 4 weeks post-implantation (scale bars = 200 μm). (E) Quantification of the CD31 + and α-SMA + area from graph D. (n = 6, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001).
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    Partial EMT phenotype proteins in HK-2 cells transfected with lncRNA NKILA overexpression virus (A) Representative western blotting images and (B) quantification of EMT phenotypic indicators. (C) Statistical analysis results of E-cad fluorescence intensity (n=3). (D) RT-qPCR statistical results of EMT phenotype indicators (n=3). ‘Normal’ indicates after starvation treatment, HK-2 cells were replaced with fresh complete medium and continued to be cultured for 24 h. Control, following starvation treatment, 10 ng/ml TGF-β1 cytokine diluent was added to induce HK-2 cells to construct the renal interstitial fibrosis model for 24 h. ‘OE-NKILA’ indicates after starvation, overexpressed Lv-NKILA (76304) was used for transfection and cells were collected after 24 h of lentivirus transfection. Compared with OE-NC ## P<0.01. E-cad; epithelial-cadherin; RT-qPCR, reverse transcription quantitative PCR; EMT, epithelial-mesenchymal transition; NC, negative control; Lv, lentivirus; OE, overexpression; FN, fibronectin; Col1, collagen I; <t>α-SMA,</t> <t>α-smooth</t> muscle actin; Vim; vimentin; ns, not significant.
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    Partial EMT phenotype proteins in HK-2 cells transfected with lncRNA NKILA overexpression virus (A) Representative western blotting images and (B) quantification of EMT phenotypic indicators. (C) Statistical analysis results of E-cad fluorescence intensity (n=3). (D) RT-qPCR statistical results of EMT phenotype indicators (n=3). ‘Normal’ indicates after starvation treatment, HK-2 cells were replaced with fresh complete medium and continued to be cultured for 24 h. Control, following starvation treatment, 10 ng/ml TGF-β1 cytokine diluent was added to induce HK-2 cells to construct the renal interstitial fibrosis model for 24 h. ‘OE-NKILA’ indicates after starvation, overexpressed Lv-NKILA (76304) was used for transfection and cells were collected after 24 h of lentivirus transfection. Compared with OE-NC ## P<0.01. E-cad; epithelial-cadherin; RT-qPCR, reverse transcription quantitative PCR; EMT, epithelial-mesenchymal transition; NC, negative control; Lv, lentivirus; OE, overexpression; FN, fibronectin; Col1, collagen I; <t>α-SMA,</t> <t>α-smooth</t> muscle actin; Vim; vimentin; ns, not significant.
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    Partial EMT phenotype proteins in HK-2 cells transfected with lncRNA NKILA overexpression virus (A) Representative western blotting images and (B) quantification of EMT phenotypic indicators. (C) Statistical analysis results of E-cad fluorescence intensity (n=3). (D) RT-qPCR statistical results of EMT phenotype indicators (n=3). ‘Normal’ indicates after starvation treatment, HK-2 cells were replaced with fresh complete medium and continued to be cultured for 24 h. Control, following starvation treatment, 10 ng/ml TGF-β1 cytokine diluent was added to induce HK-2 cells to construct the renal interstitial fibrosis model for 24 h. ‘OE-NKILA’ indicates after starvation, overexpressed Lv-NKILA (76304) was used for transfection and cells were collected after 24 h of lentivirus transfection. Compared with OE-NC ## P<0.01. E-cad; epithelial-cadherin; RT-qPCR, reverse transcription quantitative PCR; EMT, epithelial-mesenchymal transition; NC, negative control; Lv, lentivirus; OE, overexpression; FN, fibronectin; Col1, collagen I; <t>α-SMA,</t> <t>α-smooth</t> muscle actin; Vim; vimentin; ns, not significant.
    Mouse Anti α Sma, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Wuhan Sanying Biotechnology antibodies against α smooth muscle actin α sma
    Effects of CoQ10 on fibrosis-related proteins in rat lung tissue induced by SiO 2 dust suspension. ( (A) Effect of CoQ10 on HYP content in rat lungs induced by silica dust; (B) Effect of CoQ10 on the expression of EMT-related proteins in rat lungs induced by silica dust; (C) E-cad protein expression level; (D) Vimentin protein expression level; <t>(E)</t> <t>α-SMA</t> protein expression level; (F) Immunohistochemical detection <t>of</t> <t>α-SMA</t> protein expression (10×); <t>(G)</t> <t>α-SMA</t> protein positive expression level; (H) Effect of CoQ10 on collagen protein expression in rat lung tissue induced by silica dust; (I) Collagen-I protein expression level; (J) Collagen-III protein expression level. Note: * indicates P < 0.05 compared with the Control group; ** indicates P < 0.01 compared with the Control group; # indicates P < 0.05 compared with the Silicosis Model group; ## indicates P < 0.01 compared with the Silicosis Model group. All data are presented as mean ± standard deviation (M ± SD), n = 3).
    Antibodies Against α Smooth Muscle Actin α Sma, supplied by Wuhan Sanying Biotechnology, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    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

    In vivo angiogenic effects of HCH gel. (A) H&E staining of tissue sections showing the angiogenic effect after 4 weeks of hydrogel implantation. (B) Immunofluorescence co-staining for CD31 and α-SMA assessing vascular proliferation at 2 weeks post-implantation (scale bars = 200 μm). White dotted lines indicate the hydrogel–tissue interface. (C) Quantification of the CD31 + and α-SMA + area from graph B. (D) Immunofluorescence co-staining for CD31 and α-SMA at 4 weeks post-implantation (scale bars = 200 μm). (E) Quantification of the CD31 + and α-SMA + area from graph D. (n = 6, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001).

    Journal: Materials Today Bio

    Article Title: Hepatic cavernous hemangioma decellularized extracellular matrix/GelMA composite hydrogel promotes angiogenesis via the ITGA9–FAK–ERK1/2 axis

    doi: 10.1016/j.mtbio.2026.102976

    Figure Lengend Snippet: In vivo angiogenic effects of HCH gel. (A) H&E staining of tissue sections showing the angiogenic effect after 4 weeks of hydrogel implantation. (B) Immunofluorescence co-staining for CD31 and α-SMA assessing vascular proliferation at 2 weeks post-implantation (scale bars = 200 μm). White dotted lines indicate the hydrogel–tissue interface. (C) Quantification of the CD31 + and α-SMA + area from graph B. (D) Immunofluorescence co-staining for CD31 and α-SMA at 4 weeks post-implantation (scale bars = 200 μm). (E) Quantification of the CD31 + and α-SMA + area from graph D. (n = 6, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001).

    Article Snippet: Sections were then incubated overnight at 4 °C with primary antibodies against CD31 (1:100, Abcam, UK) and α-smooth muscle actin (α-SMA; 1:500, Servicebio, China).

    Techniques: In Vivo, Staining, Immunofluorescence

    Partial EMT phenotype proteins in HK-2 cells transfected with lncRNA NKILA overexpression virus (A) Representative western blotting images and (B) quantification of EMT phenotypic indicators. (C) Statistical analysis results of E-cad fluorescence intensity (n=3). (D) RT-qPCR statistical results of EMT phenotype indicators (n=3). ‘Normal’ indicates after starvation treatment, HK-2 cells were replaced with fresh complete medium and continued to be cultured for 24 h. Control, following starvation treatment, 10 ng/ml TGF-β1 cytokine diluent was added to induce HK-2 cells to construct the renal interstitial fibrosis model for 24 h. ‘OE-NKILA’ indicates after starvation, overexpressed Lv-NKILA (76304) was used for transfection and cells were collected after 24 h of lentivirus transfection. Compared with OE-NC ## P<0.01. E-cad; epithelial-cadherin; RT-qPCR, reverse transcription quantitative PCR; EMT, epithelial-mesenchymal transition; NC, negative control; Lv, lentivirus; OE, overexpression; FN, fibronectin; Col1, collagen I; α-SMA, α-smooth muscle actin; Vim; vimentin; ns, not significant.

    Journal: Molecular Medicine Reports

    Article Title: Long non-coding RNA NKILA regulates the JAK2/STAT3 pathway to exacerbate TGF-β1-mediated renal fibrosis

    doi: 10.3892/mmr.2026.13839

    Figure Lengend Snippet: Partial EMT phenotype proteins in HK-2 cells transfected with lncRNA NKILA overexpression virus (A) Representative western blotting images and (B) quantification of EMT phenotypic indicators. (C) Statistical analysis results of E-cad fluorescence intensity (n=3). (D) RT-qPCR statistical results of EMT phenotype indicators (n=3). ‘Normal’ indicates after starvation treatment, HK-2 cells were replaced with fresh complete medium and continued to be cultured for 24 h. Control, following starvation treatment, 10 ng/ml TGF-β1 cytokine diluent was added to induce HK-2 cells to construct the renal interstitial fibrosis model for 24 h. ‘OE-NKILA’ indicates after starvation, overexpressed Lv-NKILA (76304) was used for transfection and cells were collected after 24 h of lentivirus transfection. Compared with OE-NC ## P<0.01. E-cad; epithelial-cadherin; RT-qPCR, reverse transcription quantitative PCR; EMT, epithelial-mesenchymal transition; NC, negative control; Lv, lentivirus; OE, overexpression; FN, fibronectin; Col1, collagen I; α-SMA, α-smooth muscle actin; Vim; vimentin; ns, not significant.

    Article Snippet: After blocking with 5% non-fat milk for 2 h at room temperature, membranes were incubated overnight at 4°C with primary antibodies against fibronectin (FN; 1:1,000; cat. no. ab45688; Abcam), collagen I (Col1; 1:1,000; cat. no. ab138492; Abcam), vimentin (Vim; 1:1,000; cat. no. 10366-1-AP; Proteintech Group, Inc.), α-smooth muscle actin (α-SMA; 1:1,000; cat. no. 14395-1-AP; Proteintech Group, Inc.), JAK2 (1:1,000; cat. no. 17670-1-AP; Proteintech Group, Inc.), STAT3 (1:1,000; cat. no. 10253-2-AP; Proteintech Group, Inc.), phosphorylated (p)-JAK2 (1:500; cat. no. ab32101; Abcam), p-STAT3 (1:500; cat. no. ab76315; Abcam) and GAPDH (1:5,000; cat. no. 10494-1-AP; Proteintech Group, Inc.).

    Techniques: Transfection, Over Expression, Virus, Western Blot, Fluorescence, Quantitative RT-PCR, Cell Culture, Control, Construct, Reverse Transcription, Real-time Polymerase Chain Reaction, Negative Control

    Partial EMT phenotype proteins in HK-2 cells transfected with lncRNA NKILA knockdown lentivirus (A) Representative western blotting bands and (B) semi-quantification results of EMT phenotypic indicators. (C) E-cad fluorescence intensity and (D) EMT phenotypic index RT-qPCR (n=3). ‘Normal’ indicates starvation treatment. Compared with normal group ## P<0.01. Compared with control + KD-NC group, **P<0.01 and *P<0.05. EMT, epithelial-mesenchymal transition; E-cad, epithelial-cadherin; RT-qPCR, reverse transcription quantitative PCR; KD, knockdown; Lv, lentivirus; shRNA, short hairpin RNA; NC, negative control; FN, fibronectin; Col1, collagen I; α-SMA, α-smooth muscle actin; Vim; vimentin.

    Journal: Molecular Medicine Reports

    Article Title: Long non-coding RNA NKILA regulates the JAK2/STAT3 pathway to exacerbate TGF-β1-mediated renal fibrosis

    doi: 10.3892/mmr.2026.13839

    Figure Lengend Snippet: Partial EMT phenotype proteins in HK-2 cells transfected with lncRNA NKILA knockdown lentivirus (A) Representative western blotting bands and (B) semi-quantification results of EMT phenotypic indicators. (C) E-cad fluorescence intensity and (D) EMT phenotypic index RT-qPCR (n=3). ‘Normal’ indicates starvation treatment. Compared with normal group ## P<0.01. Compared with control + KD-NC group, **P<0.01 and *P<0.05. EMT, epithelial-mesenchymal transition; E-cad, epithelial-cadherin; RT-qPCR, reverse transcription quantitative PCR; KD, knockdown; Lv, lentivirus; shRNA, short hairpin RNA; NC, negative control; FN, fibronectin; Col1, collagen I; α-SMA, α-smooth muscle actin; Vim; vimentin.

    Article Snippet: After blocking with 5% non-fat milk for 2 h at room temperature, membranes were incubated overnight at 4°C with primary antibodies against fibronectin (FN; 1:1,000; cat. no. ab45688; Abcam), collagen I (Col1; 1:1,000; cat. no. ab138492; Abcam), vimentin (Vim; 1:1,000; cat. no. 10366-1-AP; Proteintech Group, Inc.), α-smooth muscle actin (α-SMA; 1:1,000; cat. no. 14395-1-AP; Proteintech Group, Inc.), JAK2 (1:1,000; cat. no. 17670-1-AP; Proteintech Group, Inc.), STAT3 (1:1,000; cat. no. 10253-2-AP; Proteintech Group, Inc.), phosphorylated (p)-JAK2 (1:500; cat. no. ab32101; Abcam), p-STAT3 (1:500; cat. no. ab76315; Abcam) and GAPDH (1:5,000; cat. no. 10494-1-AP; Proteintech Group, Inc.).

    Techniques: Transfection, Knockdown, Western Blot, Fluorescence, Quantitative RT-PCR, Control, Reverse Transcription, Real-time Polymerase Chain Reaction, shRNA, Negative Control

    Detection of EMT-related phenotypic proteins in the AG490 intervention HK-2 cell recovery experiment (A) Representative western blotting bands and (B) semi-quantification of EMT phenotypic protein changes (n=3). (C) Statistical analysis results of E-cad fluorescence intensity (n=3) and (D) EMT phenotypic index through reverse transcription quantitative PCR (n=3). ‘Normal’ indicates starvation treatment, HK-2 cells were replaced with fresh complete medium and continued to be cultured for 24 h. ## P<0.01 compared with the normal group, ** P<0.01 and *P<0.05 compared with the control + DMSO group and △△ P<0.01 and △ P<0.05 compared with the OE-NKILA group. EMT, epithelial-mesenchymal transition; E-cad, epithelial cadherin; OE, overexpression; Lv, lentivirus; FN, fibronectin; Col1, collagen I; α-SMA, α-smooth muscle actin; Vim; vimentin.

    Journal: Molecular Medicine Reports

    Article Title: Long non-coding RNA NKILA regulates the JAK2/STAT3 pathway to exacerbate TGF-β1-mediated renal fibrosis

    doi: 10.3892/mmr.2026.13839

    Figure Lengend Snippet: Detection of EMT-related phenotypic proteins in the AG490 intervention HK-2 cell recovery experiment (A) Representative western blotting bands and (B) semi-quantification of EMT phenotypic protein changes (n=3). (C) Statistical analysis results of E-cad fluorescence intensity (n=3) and (D) EMT phenotypic index through reverse transcription quantitative PCR (n=3). ‘Normal’ indicates starvation treatment, HK-2 cells were replaced with fresh complete medium and continued to be cultured for 24 h. ## P<0.01 compared with the normal group, ** P<0.01 and *P<0.05 compared with the control + DMSO group and △△ P<0.01 and △ P<0.05 compared with the OE-NKILA group. EMT, epithelial-mesenchymal transition; E-cad, epithelial cadherin; OE, overexpression; Lv, lentivirus; FN, fibronectin; Col1, collagen I; α-SMA, α-smooth muscle actin; Vim; vimentin.

    Article Snippet: After blocking with 5% non-fat milk for 2 h at room temperature, membranes were incubated overnight at 4°C with primary antibodies against fibronectin (FN; 1:1,000; cat. no. ab45688; Abcam), collagen I (Col1; 1:1,000; cat. no. ab138492; Abcam), vimentin (Vim; 1:1,000; cat. no. 10366-1-AP; Proteintech Group, Inc.), α-smooth muscle actin (α-SMA; 1:1,000; cat. no. 14395-1-AP; Proteintech Group, Inc.), JAK2 (1:1,000; cat. no. 17670-1-AP; Proteintech Group, Inc.), STAT3 (1:1,000; cat. no. 10253-2-AP; Proteintech Group, Inc.), phosphorylated (p)-JAK2 (1:500; cat. no. ab32101; Abcam), p-STAT3 (1:500; cat. no. ab76315; Abcam) and GAPDH (1:5,000; cat. no. 10494-1-AP; Proteintech Group, Inc.).

    Techniques: Cell Recovery, Western Blot, Fluorescence, Reverse Transcription, Real-time Polymerase Chain Reaction, Cell Culture, Control, Over Expression

    Effects of CoQ10 on fibrosis-related proteins in rat lung tissue induced by SiO 2 dust suspension. ( (A) Effect of CoQ10 on HYP content in rat lungs induced by silica dust; (B) Effect of CoQ10 on the expression of EMT-related proteins in rat lungs induced by silica dust; (C) E-cad protein expression level; (D) Vimentin protein expression level; (E) α-SMA protein expression level; (F) Immunohistochemical detection of α-SMA protein expression (10×); (G) α-SMA protein positive expression level; (H) Effect of CoQ10 on collagen protein expression in rat lung tissue induced by silica dust; (I) Collagen-I protein expression level; (J) Collagen-III protein expression level. Note: * indicates P < 0.05 compared with the Control group; ** indicates P < 0.01 compared with the Control group; # indicates P < 0.05 compared with the Silicosis Model group; ## indicates P < 0.01 compared with the Silicosis Model group. All data are presented as mean ± standard deviation (M ± SD), n = 3).

    Journal: Frontiers in Pharmacology

    Article Title: Coenzyme Q10 alleviates silicotic fibrosis in rats through the TGF-β1/Smad pathway

    doi: 10.3389/fphar.2026.1821205

    Figure Lengend Snippet: Effects of CoQ10 on fibrosis-related proteins in rat lung tissue induced by SiO 2 dust suspension. ( (A) Effect of CoQ10 on HYP content in rat lungs induced by silica dust; (B) Effect of CoQ10 on the expression of EMT-related proteins in rat lungs induced by silica dust; (C) E-cad protein expression level; (D) Vimentin protein expression level; (E) α-SMA protein expression level; (F) Immunohistochemical detection of α-SMA protein expression (10×); (G) α-SMA protein positive expression level; (H) Effect of CoQ10 on collagen protein expression in rat lung tissue induced by silica dust; (I) Collagen-I protein expression level; (J) Collagen-III protein expression level. Note: * indicates P < 0.05 compared with the Control group; ** indicates P < 0.01 compared with the Control group; # indicates P < 0.05 compared with the Silicosis Model group; ## indicates P < 0.01 compared with the Silicosis Model group. All data are presented as mean ± standard deviation (M ± SD), n = 3).

    Article Snippet: Free silica dust (SiO 2 , with ≥80% of particles measuring 0.5–5 μm, Sigma-Aldrich, United States); Coenzyme Q10 (Macklin Biochemical Technology Co., Ltd., Shanghai, China); Kits for Interleukin-1β (IL-1β), Tumor Necrosis Factor-α (TNF-α), Superoxide Dismutase (SOD), and Malondialdehyde (MDA) (Nanjing Jiancheng Bioengineering Institute, China); Hematoxylin and Eosin (H&E) staining solution, Mayer’s Hematoxylin, Eosin Y solution, Masson’s Trichrome Stain Kit, Reactive Oxygen Species (ROS) Staining Kit (Wuhan Biqindu Biotechnology Co., Ltd., China); Tween 20, Rapid Wright-Giemsa Stain, Bicinchoninic Acid (BCA) Protein Assay Kit (Beijing Dingguo Changsheng Biotechnology Co., Ltd., China); Antibodies against α-Smooth Muscle Actin (α-SMA), E-cadherin (E-cad), Vimentin, Collagen Type III (Col-III), Smad2, Smad3 (Abclonal Technology Co., Ltd., Wuhan, China); Antibodies against Collagen Type I (Col-I), Smad7 (Wuhan Sanying Biotechnology Co., Ltd., China); Antibody against Transforming Growth Factor Beta 1 (TGF-β1) (Abcam, China); Horseradish Peroxidase (HRP)-conjugated Goat Anti-Rabbit antibody (Abclonal, China).

    Techniques: Suspension, Expressing, Immunohistochemical staining, Control, Standard Deviation