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rabbit anti-mouse alpha smooth muscle actin (α-sma  (Servicebio Inc)

 
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    Structured Review

    Servicebio Inc rabbit anti-mouse alpha smooth muscle actin (α-sma
    Thymic stromal lymphopoietin (TSLP) levels are elevated in cardiac tissues following myocardial infarction (MI). (A) MI was induced in C57/B6J mice in vivo and western blotting analysis of TSLP expression in heart tissues was performed on day 7 later, using β-actin as a loading control; each lane represents an independent mouse heart (n = 5 per group). (B) Tlsp mRNA levels in the heart tissues of mice on day 7 post-MI. Transcripts were normalized to glyceraldehyde-3-phosphate dehydrogenase ( Gapdh ) (n = 7 per group). (C) A representative western blotting analysis was conducted to assess TSLP expression in mouse cardiac tissues at baseline (BL) and day 1, day 7, day 14, and day 28 post-MI (n =5–8 per group). (D) Tslp mRNA expression was evaluated in myocardial cells isolated using the Langendorff perfusion system from mice in both the MI and sham groups on day 7 post-surgery (n = 7 per group). (E) TSLP representative immunofluorescence staining in myocardial tissues of mice on day 7 post-MI: TSLP (red), α-actinin (green, upper left images), <t>CD31</t> (green, upper right images), alpha smooth muscle actin (α-SMA; green, bottom left images), and vimentin (green, bottom right images). The sections were counterstained with 4’,6-diamidino-2-phenylindole (DAPI) to visualize nuclei (blue; scale bar: 50 μm) (n = 5 per group). (F, G) Surface expression of TSLP receptor (TSLPR) on CD4 + T cells, T regulatory (Treg) cells, dendritic cells, neutrophils and monocytes/macrophages (Mono/Macro) in the spleen and heart on day 7 post-MI (n = 4–9 per group). Mann–Whitney U test was used to analyze the data in (A, B, D) , whereas the data in (C, F, G) were analyzed using one-way ANOVA, followed by Tukey’s multiple comparisons test. * P< 0.05 compared with BL; # P< 0.05 compared with 1D.
    Rabbit Anti Mouse Alpha Smooth Muscle Actin (α Sma, supplied by Servicebio Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti-mouse alpha smooth muscle actin (α-sma/product/Servicebio Inc
    Average 90 stars, based on 1 article reviews
    rabbit anti-mouse alpha smooth muscle actin (α-sma - by Bioz Stars, 2026-02
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    Images

    1) Product Images from "Thymic stromal lymphopoietin modulates T cell response and improves cardiac repair post-myocardial infarction"

    Article Title: Thymic stromal lymphopoietin modulates T cell response and improves cardiac repair post-myocardial infarction

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2024.1467095

    Thymic stromal lymphopoietin (TSLP) levels are elevated in cardiac tissues following myocardial infarction (MI). (A) MI was induced in C57/B6J mice in vivo and western blotting analysis of TSLP expression in heart tissues was performed on day 7 later, using β-actin as a loading control; each lane represents an independent mouse heart (n = 5 per group). (B) Tlsp mRNA levels in the heart tissues of mice on day 7 post-MI. Transcripts were normalized to glyceraldehyde-3-phosphate dehydrogenase ( Gapdh ) (n = 7 per group). (C) A representative western blotting analysis was conducted to assess TSLP expression in mouse cardiac tissues at baseline (BL) and day 1, day 7, day 14, and day 28 post-MI (n =5–8 per group). (D) Tslp mRNA expression was evaluated in myocardial cells isolated using the Langendorff perfusion system from mice in both the MI and sham groups on day 7 post-surgery (n = 7 per group). (E) TSLP representative immunofluorescence staining in myocardial tissues of mice on day 7 post-MI: TSLP (red), α-actinin (green, upper left images), CD31 (green, upper right images), alpha smooth muscle actin (α-SMA; green, bottom left images), and vimentin (green, bottom right images). The sections were counterstained with 4’,6-diamidino-2-phenylindole (DAPI) to visualize nuclei (blue; scale bar: 50 μm) (n = 5 per group). (F, G) Surface expression of TSLP receptor (TSLPR) on CD4 + T cells, T regulatory (Treg) cells, dendritic cells, neutrophils and monocytes/macrophages (Mono/Macro) in the spleen and heart on day 7 post-MI (n = 4–9 per group). Mann–Whitney U test was used to analyze the data in (A, B, D) , whereas the data in (C, F, G) were analyzed using one-way ANOVA, followed by Tukey’s multiple comparisons test. * P< 0.05 compared with BL; # P< 0.05 compared with 1D.
    Figure Legend Snippet: Thymic stromal lymphopoietin (TSLP) levels are elevated in cardiac tissues following myocardial infarction (MI). (A) MI was induced in C57/B6J mice in vivo and western blotting analysis of TSLP expression in heart tissues was performed on day 7 later, using β-actin as a loading control; each lane represents an independent mouse heart (n = 5 per group). (B) Tlsp mRNA levels in the heart tissues of mice on day 7 post-MI. Transcripts were normalized to glyceraldehyde-3-phosphate dehydrogenase ( Gapdh ) (n = 7 per group). (C) A representative western blotting analysis was conducted to assess TSLP expression in mouse cardiac tissues at baseline (BL) and day 1, day 7, day 14, and day 28 post-MI (n =5–8 per group). (D) Tslp mRNA expression was evaluated in myocardial cells isolated using the Langendorff perfusion system from mice in both the MI and sham groups on day 7 post-surgery (n = 7 per group). (E) TSLP representative immunofluorescence staining in myocardial tissues of mice on day 7 post-MI: TSLP (red), α-actinin (green, upper left images), CD31 (green, upper right images), alpha smooth muscle actin (α-SMA; green, bottom left images), and vimentin (green, bottom right images). The sections were counterstained with 4’,6-diamidino-2-phenylindole (DAPI) to visualize nuclei (blue; scale bar: 50 μm) (n = 5 per group). (F, G) Surface expression of TSLP receptor (TSLPR) on CD4 + T cells, T regulatory (Treg) cells, dendritic cells, neutrophils and monocytes/macrophages (Mono/Macro) in the spleen and heart on day 7 post-MI (n = 4–9 per group). Mann–Whitney U test was used to analyze the data in (A, B, D) , whereas the data in (C, F, G) were analyzed using one-way ANOVA, followed by Tukey’s multiple comparisons test. * P< 0.05 compared with BL; # P< 0.05 compared with 1D.

    Techniques Used: In Vivo, Western Blot, Expressing, Control, Isolation, Immunofluorescence, Staining, MANN-WHITNEY

    The absence of the thymic stromal lymphopoietin (TSLP)/TSLP receptor (TSLPR) signaling pathway aggravates ventricular remodeling following myocardium infarction (MI) in mice. (A) Heart sections were stained with Masson’s trichrome to obtain representative images (scale bar: 2 mm). (B, C) Quantitative analyses of infarct size and scar thickness on day 28 post-MI (n = 10 per group). (D, E) Representative images showing collagen volume (blue) in the border zone and quantification of the collagen volume fraction (CVF) per high-power field after Masson’s trichrome staining on day 28 post-MI (scale bar: 100 μm) (n=8 per group). (F, G) Representative images showing CD31 + staining in the peri-infarct region on day 7 post-MI (scale bar: 20 μm) and quantification of the CD31 + area (n = 10 per group). (H, I) Representative images showing WGA staining in the remote region on 28 days post- MI (scale bar: 20 μm) and quantification of the average myocardial area (n = 8–9 per group). Data are presented as the mean ± SEM. The Mann–Whitney U test was utilized to analyze the data in (B, E) , while unpaired t-test was employed for statistical analysis in (C, G, I) .
    Figure Legend Snippet: The absence of the thymic stromal lymphopoietin (TSLP)/TSLP receptor (TSLPR) signaling pathway aggravates ventricular remodeling following myocardium infarction (MI) in mice. (A) Heart sections were stained with Masson’s trichrome to obtain representative images (scale bar: 2 mm). (B, C) Quantitative analyses of infarct size and scar thickness on day 28 post-MI (n = 10 per group). (D, E) Representative images showing collagen volume (blue) in the border zone and quantification of the collagen volume fraction (CVF) per high-power field after Masson’s trichrome staining on day 28 post-MI (scale bar: 100 μm) (n=8 per group). (F, G) Representative images showing CD31 + staining in the peri-infarct region on day 7 post-MI (scale bar: 20 μm) and quantification of the CD31 + area (n = 10 per group). (H, I) Representative images showing WGA staining in the remote region on 28 days post- MI (scale bar: 20 μm) and quantification of the average myocardial area (n = 8–9 per group). Data are presented as the mean ± SEM. The Mann–Whitney U test was utilized to analyze the data in (B, E) , while unpaired t-test was employed for statistical analysis in (C, G, I) .

    Techniques Used: Staining, MANN-WHITNEY



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    Image Search Results


    Thymic stromal lymphopoietin (TSLP) levels are elevated in cardiac tissues following myocardial infarction (MI). (A) MI was induced in C57/B6J mice in vivo and western blotting analysis of TSLP expression in heart tissues was performed on day 7 later, using β-actin as a loading control; each lane represents an independent mouse heart (n = 5 per group). (B) Tlsp mRNA levels in the heart tissues of mice on day 7 post-MI. Transcripts were normalized to glyceraldehyde-3-phosphate dehydrogenase ( Gapdh ) (n = 7 per group). (C) A representative western blotting analysis was conducted to assess TSLP expression in mouse cardiac tissues at baseline (BL) and day 1, day 7, day 14, and day 28 post-MI (n =5–8 per group). (D) Tslp mRNA expression was evaluated in myocardial cells isolated using the Langendorff perfusion system from mice in both the MI and sham groups on day 7 post-surgery (n = 7 per group). (E) TSLP representative immunofluorescence staining in myocardial tissues of mice on day 7 post-MI: TSLP (red), α-actinin (green, upper left images), CD31 (green, upper right images), alpha smooth muscle actin (α-SMA; green, bottom left images), and vimentin (green, bottom right images). The sections were counterstained with 4’,6-diamidino-2-phenylindole (DAPI) to visualize nuclei (blue; scale bar: 50 μm) (n = 5 per group). (F, G) Surface expression of TSLP receptor (TSLPR) on CD4 + T cells, T regulatory (Treg) cells, dendritic cells, neutrophils and monocytes/macrophages (Mono/Macro) in the spleen and heart on day 7 post-MI (n = 4–9 per group). Mann–Whitney U test was used to analyze the data in (A, B, D) , whereas the data in (C, F, G) were analyzed using one-way ANOVA, followed by Tukey’s multiple comparisons test. * P< 0.05 compared with BL; # P< 0.05 compared with 1D.

    Journal: Frontiers in Immunology

    Article Title: Thymic stromal lymphopoietin modulates T cell response and improves cardiac repair post-myocardial infarction

    doi: 10.3389/fimmu.2024.1467095

    Figure Lengend Snippet: Thymic stromal lymphopoietin (TSLP) levels are elevated in cardiac tissues following myocardial infarction (MI). (A) MI was induced in C57/B6J mice in vivo and western blotting analysis of TSLP expression in heart tissues was performed on day 7 later, using β-actin as a loading control; each lane represents an independent mouse heart (n = 5 per group). (B) Tlsp mRNA levels in the heart tissues of mice on day 7 post-MI. Transcripts were normalized to glyceraldehyde-3-phosphate dehydrogenase ( Gapdh ) (n = 7 per group). (C) A representative western blotting analysis was conducted to assess TSLP expression in mouse cardiac tissues at baseline (BL) and day 1, day 7, day 14, and day 28 post-MI (n =5–8 per group). (D) Tslp mRNA expression was evaluated in myocardial cells isolated using the Langendorff perfusion system from mice in both the MI and sham groups on day 7 post-surgery (n = 7 per group). (E) TSLP representative immunofluorescence staining in myocardial tissues of mice on day 7 post-MI: TSLP (red), α-actinin (green, upper left images), CD31 (green, upper right images), alpha smooth muscle actin (α-SMA; green, bottom left images), and vimentin (green, bottom right images). The sections were counterstained with 4’,6-diamidino-2-phenylindole (DAPI) to visualize nuclei (blue; scale bar: 50 μm) (n = 5 per group). (F, G) Surface expression of TSLP receptor (TSLPR) on CD4 + T cells, T regulatory (Treg) cells, dendritic cells, neutrophils and monocytes/macrophages (Mono/Macro) in the spleen and heart on day 7 post-MI (n = 4–9 per group). Mann–Whitney U test was used to analyze the data in (A, B, D) , whereas the data in (C, F, G) were analyzed using one-way ANOVA, followed by Tukey’s multiple comparisons test. * P< 0.05 compared with BL; # P< 0.05 compared with 1D.

    Article Snippet: Slices were stained with rabbit anti-mouse TSLP, rabbit anti-mouse CD31, rabbit anti-mouse alpha smooth muscle actin (α-SMA), rabbit anti-mouse vimentin, rabbit anti-mouse actinin (all above antibodies from Servicebio, Wuhan, China), and goat anti-rabbit secondary antibodies (Servicebio, Wuhan, China).

    Techniques: In Vivo, Western Blot, Expressing, Control, Isolation, Immunofluorescence, Staining, MANN-WHITNEY

    The absence of the thymic stromal lymphopoietin (TSLP)/TSLP receptor (TSLPR) signaling pathway aggravates ventricular remodeling following myocardium infarction (MI) in mice. (A) Heart sections were stained with Masson’s trichrome to obtain representative images (scale bar: 2 mm). (B, C) Quantitative analyses of infarct size and scar thickness on day 28 post-MI (n = 10 per group). (D, E) Representative images showing collagen volume (blue) in the border zone and quantification of the collagen volume fraction (CVF) per high-power field after Masson’s trichrome staining on day 28 post-MI (scale bar: 100 μm) (n=8 per group). (F, G) Representative images showing CD31 + staining in the peri-infarct region on day 7 post-MI (scale bar: 20 μm) and quantification of the CD31 + area (n = 10 per group). (H, I) Representative images showing WGA staining in the remote region on 28 days post- MI (scale bar: 20 μm) and quantification of the average myocardial area (n = 8–9 per group). Data are presented as the mean ± SEM. The Mann–Whitney U test was utilized to analyze the data in (B, E) , while unpaired t-test was employed for statistical analysis in (C, G, I) .

    Journal: Frontiers in Immunology

    Article Title: Thymic stromal lymphopoietin modulates T cell response and improves cardiac repair post-myocardial infarction

    doi: 10.3389/fimmu.2024.1467095

    Figure Lengend Snippet: The absence of the thymic stromal lymphopoietin (TSLP)/TSLP receptor (TSLPR) signaling pathway aggravates ventricular remodeling following myocardium infarction (MI) in mice. (A) Heart sections were stained with Masson’s trichrome to obtain representative images (scale bar: 2 mm). (B, C) Quantitative analyses of infarct size and scar thickness on day 28 post-MI (n = 10 per group). (D, E) Representative images showing collagen volume (blue) in the border zone and quantification of the collagen volume fraction (CVF) per high-power field after Masson’s trichrome staining on day 28 post-MI (scale bar: 100 μm) (n=8 per group). (F, G) Representative images showing CD31 + staining in the peri-infarct region on day 7 post-MI (scale bar: 20 μm) and quantification of the CD31 + area (n = 10 per group). (H, I) Representative images showing WGA staining in the remote region on 28 days post- MI (scale bar: 20 μm) and quantification of the average myocardial area (n = 8–9 per group). Data are presented as the mean ± SEM. The Mann–Whitney U test was utilized to analyze the data in (B, E) , while unpaired t-test was employed for statistical analysis in (C, G, I) .

    Article Snippet: Slices were stained with rabbit anti-mouse TSLP, rabbit anti-mouse CD31, rabbit anti-mouse alpha smooth muscle actin (α-SMA), rabbit anti-mouse vimentin, rabbit anti-mouse actinin (all above antibodies from Servicebio, Wuhan, China), and goat anti-rabbit secondary antibodies (Servicebio, Wuhan, China).

    Techniques: Staining, MANN-WHITNEY

    Collateral formation of mice with either standard diet (SD), high-fat diet-induced obesity (DIO), low-dose streptozotocin (STZ)-induced hyperglycemia, or type 2 diabetes (T2D) induced by both DIO plus low-dose STZ injections after hindlimb ischemia. After the animal models of chronic conditions, including hyperglycemia induced by low-dose STZ injections, DIO, and T2D induced by DIO-STZ using SD plus vehicle (citrate buffer) injection as healthy control, was developed, hind limb ischemia was created in these animals by unilateral artery ligation. ( A ) The adductor muscle was collected at the end of the study and performed α-Smooth muscle actin (αSMA, red) and CD31 staining (green). Scale bar, 400 μm. The quantification of arterial density ( B ) and diameter ( C ) are shown. * p < 0.05. ns, not significant. ( D ) The calf muscle was collected and stained with CD31 antibody. Scale bar, 400 μm. The quantification of capillary density is shown in ( E ). When a comparison was made between the two groups, the p values were determined by the Mann–Whitney U test. When comparison was made between more than two groups of treatments, the p values were first determined by the Kruskal–Wallis test across all the groups and, if significant, the pairs of primary interest, based on scientific rationale, were assessed using the Mann–Whitney U test with Benjamini Krieger, and Yekutieli’s adjustment for multiple comparisons. The significant differences that came from post hoc comparisons of groups were noted.

    Journal: International Journal of Molecular Sciences

    Article Title: The Impact of Obesity on Diabetes Onset and Neovascularization in Mouse Models of Metabolic Stress

    doi: 10.3390/ijms25021214

    Figure Lengend Snippet: Collateral formation of mice with either standard diet (SD), high-fat diet-induced obesity (DIO), low-dose streptozotocin (STZ)-induced hyperglycemia, or type 2 diabetes (T2D) induced by both DIO plus low-dose STZ injections after hindlimb ischemia. After the animal models of chronic conditions, including hyperglycemia induced by low-dose STZ injections, DIO, and T2D induced by DIO-STZ using SD plus vehicle (citrate buffer) injection as healthy control, was developed, hind limb ischemia was created in these animals by unilateral artery ligation. ( A ) The adductor muscle was collected at the end of the study and performed α-Smooth muscle actin (αSMA, red) and CD31 staining (green). Scale bar, 400 μm. The quantification of arterial density ( B ) and diameter ( C ) are shown. * p < 0.05. ns, not significant. ( D ) The calf muscle was collected and stained with CD31 antibody. Scale bar, 400 μm. The quantification of capillary density is shown in ( E ). When a comparison was made between the two groups, the p values were determined by the Mann–Whitney U test. When comparison was made between more than two groups of treatments, the p values were first determined by the Kruskal–Wallis test across all the groups and, if significant, the pairs of primary interest, based on scientific rationale, were assessed using the Mann–Whitney U test with Benjamini Krieger, and Yekutieli’s adjustment for multiple comparisons. The significant differences that came from post hoc comparisons of groups were noted.

    Article Snippet: The sections were incubated with a goat anti-mouse CD31 conjugated Alexa 488 antibody (R&D Systems, Minneapolis, MN, USA, #FAB 3628G) or incubated with a goat anti-mouse α smooth muscle actin (SMA) conjugated Alexa 594 antibody (Cell Signaling Technology, Danvers, MA, USA, #36110).

    Techniques: Injection, Control, Ligation, Staining, Comparison, MANN-WHITNEY