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staining for cardiomyocyte  (Bioss)


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    Structured Review

    Bioss staining for cardiomyocyte
    Chymase mMCP4 expression and function in mice after MI injury. A. Western blot analysis of mouse chymase mMCP4 expression in sham-operated and 28 days post-MI hearts from WT mice. B. Immunofluorescent double staining colocalized mMCP4-positive cells to myosin heavy chain-positive <t>cardiomyocytes</t> in the infarct, border, and remote regions in WT mice at 28 days post-MI. C. Immunofluorescent double staining showed mMCP4 expression in α-SMA-positive fibroblasts and Mac-2-positive macrophages in the infarct regions from 28 days post-MI heart. Scale: 200 μm, inset scale: 70 μm. D. Mortality rate of both WT and Mcpt4−/− mice during the course of 28 days of post-MI recovery. Kaplan-Meier survival analysis with log-rank test. E. Infarct sizes of both WT and Mcpt4−/− mice at 3 days and 28 days post-MI. Representative M-mode echocardiography images (F), ejection fraction (EF) (G), fractional shortening (FS) (H), body weight, heart weight, and heart-to-body weight ratio (I), LV diastole and systole volumes (J), and LV diastole and systole internal diameters (K) of WT and Mcpt4−/− mice at 28 days after sham operation or MI. The mouse numbers and genotypes are indicated in the legends. P<0.05 was considered statistically significant, independent t-test or one-way ANOVA with post-hoc Bonferroni test. Data are mean±SEM.
    Staining For Cardiomyocyte, supplied by Bioss, used in various techniques. Bioz Stars score: 91/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Deficiency of mouse mast cell protease 4 mitigates cardiac dysfunctions in mice after myocardium infarction"

    Article Title: Deficiency of mouse mast cell protease 4 mitigates cardiac dysfunctions in mice after myocardium infarction

    Journal: Biochimica et biophysica acta. Molecular basis of disease

    doi: 10.1016/j.bbadis.2019.01.011

    Chymase mMCP4 expression and function in mice after MI injury. A. Western blot analysis of mouse chymase mMCP4 expression in sham-operated and 28 days post-MI hearts from WT mice. B. Immunofluorescent double staining colocalized mMCP4-positive cells to myosin heavy chain-positive cardiomyocytes in the infarct, border, and remote regions in WT mice at 28 days post-MI. C. Immunofluorescent double staining showed mMCP4 expression in α-SMA-positive fibroblasts and Mac-2-positive macrophages in the infarct regions from 28 days post-MI heart. Scale: 200 μm, inset scale: 70 μm. D. Mortality rate of both WT and Mcpt4−/− mice during the course of 28 days of post-MI recovery. Kaplan-Meier survival analysis with log-rank test. E. Infarct sizes of both WT and Mcpt4−/− mice at 3 days and 28 days post-MI. Representative M-mode echocardiography images (F), ejection fraction (EF) (G), fractional shortening (FS) (H), body weight, heart weight, and heart-to-body weight ratio (I), LV diastole and systole volumes (J), and LV diastole and systole internal diameters (K) of WT and Mcpt4−/− mice at 28 days after sham operation or MI. The mouse numbers and genotypes are indicated in the legends. P<0.05 was considered statistically significant, independent t-test or one-way ANOVA with post-hoc Bonferroni test. Data are mean±SEM.
    Figure Legend Snippet: Chymase mMCP4 expression and function in mice after MI injury. A. Western blot analysis of mouse chymase mMCP4 expression in sham-operated and 28 days post-MI hearts from WT mice. B. Immunofluorescent double staining colocalized mMCP4-positive cells to myosin heavy chain-positive cardiomyocytes in the infarct, border, and remote regions in WT mice at 28 days post-MI. C. Immunofluorescent double staining showed mMCP4 expression in α-SMA-positive fibroblasts and Mac-2-positive macrophages in the infarct regions from 28 days post-MI heart. Scale: 200 μm, inset scale: 70 μm. D. Mortality rate of both WT and Mcpt4−/− mice during the course of 28 days of post-MI recovery. Kaplan-Meier survival analysis with log-rank test. E. Infarct sizes of both WT and Mcpt4−/− mice at 3 days and 28 days post-MI. Representative M-mode echocardiography images (F), ejection fraction (EF) (G), fractional shortening (FS) (H), body weight, heart weight, and heart-to-body weight ratio (I), LV diastole and systole volumes (J), and LV diastole and systole internal diameters (K) of WT and Mcpt4−/− mice at 28 days after sham operation or MI. The mouse numbers and genotypes are indicated in the legends. P<0.05 was considered statistically significant, independent t-test or one-way ANOVA with post-hoc Bonferroni test. Data are mean±SEM.

    Techniques Used: Expressing, Western Blot, Double Staining

    Cell apoptosis in post-MI myocardium. A. Immunofluorescent double staining colocalized cleaved caspase 3-positive cells to myosin heavy chain-positive cardiomyocytes in infarct, border, and remote regions from WT (top panels) and Mcpt4−/− mice (bottom panels) at 28 days post-MI. B. Quantification of apoptotic cardiomyocytes in infarct, border, and remote regions. C. Immunofluorescent double staining colocalized cleaved caspase 3-positive cells to α-SMA-positive fibroblasts in infarct, border, and remote regions from WT (top panels) and Mcpt4−/− mice (bottom panels) at 28 days post-MI. D. Quantification of fibroblast apoptosis in infarct, border, and remote regions. Scale: 200 μm, inset scale: 70 μm. Data are representative of 6~8 specimens per genotype. P<0.05 was considered statistically significant, independent t-test. Data are mean±SEM.
    Figure Legend Snippet: Cell apoptosis in post-MI myocardium. A. Immunofluorescent double staining colocalized cleaved caspase 3-positive cells to myosin heavy chain-positive cardiomyocytes in infarct, border, and remote regions from WT (top panels) and Mcpt4−/− mice (bottom panels) at 28 days post-MI. B. Quantification of apoptotic cardiomyocytes in infarct, border, and remote regions. C. Immunofluorescent double staining colocalized cleaved caspase 3-positive cells to α-SMA-positive fibroblasts in infarct, border, and remote regions from WT (top panels) and Mcpt4−/− mice (bottom panels) at 28 days post-MI. D. Quantification of fibroblast apoptosis in infarct, border, and remote regions. Scale: 200 μm, inset scale: 70 μm. Data are representative of 6~8 specimens per genotype. P<0.05 was considered statistically significant, independent t-test. Data are mean±SEM.

    Techniques Used: Double Staining

    Role of mMCP4 in cardiomyocyte apoptosis. A/B. Representative FACS analysis and quantification of Annexin V+PI− early apoptotic cardiomyocytes and Annexin V+PI+ late apoptotic cardiomyocytes from WT and Mcpt4−/− mice after cells were treated with and without (Control) H2O2. C/D. Annexin V and PI immunofluorescent staining representative images and apoptosis quantification of cardiomyocytes from WT and Mcpt4−/− mice with and without 100 μM H2O2 treatment. Data are mean±SEM from six independent experiments. Scale: 200 μm, inset scale: 70 μm. E. Immunoblot analysis of Bax, Bid, and tBid in cardiomyocytes from WT and Mcpt4−/− mice after cells were treated with or without H2O2. F. Immunoblot analysis of CatS, CatK, CatL, and CatB in cardiomyocytes from WT and Mcpt4−/− mice after cells were treated with or without H2O2. The same blots were reprobed for β-Actin to ensure equal protein loading. Immunoblot data are representative of three independent experiments. P<0.05 was considered statistically significant, independent t-test or one-way ANOVA with post-hoc Bonferroni test. Data are mean±SEM.
    Figure Legend Snippet: Role of mMCP4 in cardiomyocyte apoptosis. A/B. Representative FACS analysis and quantification of Annexin V+PI− early apoptotic cardiomyocytes and Annexin V+PI+ late apoptotic cardiomyocytes from WT and Mcpt4−/− mice after cells were treated with and without (Control) H2O2. C/D. Annexin V and PI immunofluorescent staining representative images and apoptosis quantification of cardiomyocytes from WT and Mcpt4−/− mice with and without 100 μM H2O2 treatment. Data are mean±SEM from six independent experiments. Scale: 200 μm, inset scale: 70 μm. E. Immunoblot analysis of Bax, Bid, and tBid in cardiomyocytes from WT and Mcpt4−/− mice after cells were treated with or without H2O2. F. Immunoblot analysis of CatS, CatK, CatL, and CatB in cardiomyocytes from WT and Mcpt4−/− mice after cells were treated with or without H2O2. The same blots were reprobed for β-Actin to ensure equal protein loading. Immunoblot data are representative of three independent experiments. P<0.05 was considered statistically significant, independent t-test or one-way ANOVA with post-hoc Bonferroni test. Data are mean±SEM.

    Techniques Used: Staining, Western Blot



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    Image Search Results


    Chymase mMCP4 expression and function in mice after MI injury. A. Western blot analysis of mouse chymase mMCP4 expression in sham-operated and 28 days post-MI hearts from WT mice. B. Immunofluorescent double staining colocalized mMCP4-positive cells to myosin heavy chain-positive cardiomyocytes in the infarct, border, and remote regions in WT mice at 28 days post-MI. C. Immunofluorescent double staining showed mMCP4 expression in α-SMA-positive fibroblasts and Mac-2-positive macrophages in the infarct regions from 28 days post-MI heart. Scale: 200 μm, inset scale: 70 μm. D. Mortality rate of both WT and Mcpt4−/− mice during the course of 28 days of post-MI recovery. Kaplan-Meier survival analysis with log-rank test. E. Infarct sizes of both WT and Mcpt4−/− mice at 3 days and 28 days post-MI. Representative M-mode echocardiography images (F), ejection fraction (EF) (G), fractional shortening (FS) (H), body weight, heart weight, and heart-to-body weight ratio (I), LV diastole and systole volumes (J), and LV diastole and systole internal diameters (K) of WT and Mcpt4−/− mice at 28 days after sham operation or MI. The mouse numbers and genotypes are indicated in the legends. P<0.05 was considered statistically significant, independent t-test or one-way ANOVA with post-hoc Bonferroni test. Data are mean±SEM.

    Journal: Biochimica et biophysica acta. Molecular basis of disease

    Article Title: Deficiency of mouse mast cell protease 4 mitigates cardiac dysfunctions in mice after myocardium infarction

    doi: 10.1016/j.bbadis.2019.01.011

    Figure Lengend Snippet: Chymase mMCP4 expression and function in mice after MI injury. A. Western blot analysis of mouse chymase mMCP4 expression in sham-operated and 28 days post-MI hearts from WT mice. B. Immunofluorescent double staining colocalized mMCP4-positive cells to myosin heavy chain-positive cardiomyocytes in the infarct, border, and remote regions in WT mice at 28 days post-MI. C. Immunofluorescent double staining showed mMCP4 expression in α-SMA-positive fibroblasts and Mac-2-positive macrophages in the infarct regions from 28 days post-MI heart. Scale: 200 μm, inset scale: 70 μm. D. Mortality rate of both WT and Mcpt4−/− mice during the course of 28 days of post-MI recovery. Kaplan-Meier survival analysis with log-rank test. E. Infarct sizes of both WT and Mcpt4−/− mice at 3 days and 28 days post-MI. Representative M-mode echocardiography images (F), ejection fraction (EF) (G), fractional shortening (FS) (H), body weight, heart weight, and heart-to-body weight ratio (I), LV diastole and systole volumes (J), and LV diastole and systole internal diameters (K) of WT and Mcpt4−/− mice at 28 days after sham operation or MI. The mouse numbers and genotypes are indicated in the legends. P<0.05 was considered statistically significant, independent t-test or one-way ANOVA with post-hoc Bonferroni test. Data are mean±SEM.

    Article Snippet: Immunofluorescent, immunohistological, and Masson’s trichrome staining To localize apoptotic cells and detect the expression of mMCP4 in the heart, heart frozen sections (6 μm) were used for immunofluorescent staining for cardiomyocyte (myosin heavy chain, 1:50, Cat# bs-15444R-A488, Bioss In.

    Techniques: Expressing, Western Blot, Double Staining

    Cell apoptosis in post-MI myocardium. A. Immunofluorescent double staining colocalized cleaved caspase 3-positive cells to myosin heavy chain-positive cardiomyocytes in infarct, border, and remote regions from WT (top panels) and Mcpt4−/− mice (bottom panels) at 28 days post-MI. B. Quantification of apoptotic cardiomyocytes in infarct, border, and remote regions. C. Immunofluorescent double staining colocalized cleaved caspase 3-positive cells to α-SMA-positive fibroblasts in infarct, border, and remote regions from WT (top panels) and Mcpt4−/− mice (bottom panels) at 28 days post-MI. D. Quantification of fibroblast apoptosis in infarct, border, and remote regions. Scale: 200 μm, inset scale: 70 μm. Data are representative of 6~8 specimens per genotype. P<0.05 was considered statistically significant, independent t-test. Data are mean±SEM.

    Journal: Biochimica et biophysica acta. Molecular basis of disease

    Article Title: Deficiency of mouse mast cell protease 4 mitigates cardiac dysfunctions in mice after myocardium infarction

    doi: 10.1016/j.bbadis.2019.01.011

    Figure Lengend Snippet: Cell apoptosis in post-MI myocardium. A. Immunofluorescent double staining colocalized cleaved caspase 3-positive cells to myosin heavy chain-positive cardiomyocytes in infarct, border, and remote regions from WT (top panels) and Mcpt4−/− mice (bottom panels) at 28 days post-MI. B. Quantification of apoptotic cardiomyocytes in infarct, border, and remote regions. C. Immunofluorescent double staining colocalized cleaved caspase 3-positive cells to α-SMA-positive fibroblasts in infarct, border, and remote regions from WT (top panels) and Mcpt4−/− mice (bottom panels) at 28 days post-MI. D. Quantification of fibroblast apoptosis in infarct, border, and remote regions. Scale: 200 μm, inset scale: 70 μm. Data are representative of 6~8 specimens per genotype. P<0.05 was considered statistically significant, independent t-test. Data are mean±SEM.

    Article Snippet: Immunofluorescent, immunohistological, and Masson’s trichrome staining To localize apoptotic cells and detect the expression of mMCP4 in the heart, heart frozen sections (6 μm) were used for immunofluorescent staining for cardiomyocyte (myosin heavy chain, 1:50, Cat# bs-15444R-A488, Bioss In.

    Techniques: Double Staining

    Role of mMCP4 in cardiomyocyte apoptosis. A/B. Representative FACS analysis and quantification of Annexin V+PI− early apoptotic cardiomyocytes and Annexin V+PI+ late apoptotic cardiomyocytes from WT and Mcpt4−/− mice after cells were treated with and without (Control) H2O2. C/D. Annexin V and PI immunofluorescent staining representative images and apoptosis quantification of cardiomyocytes from WT and Mcpt4−/− mice with and without 100 μM H2O2 treatment. Data are mean±SEM from six independent experiments. Scale: 200 μm, inset scale: 70 μm. E. Immunoblot analysis of Bax, Bid, and tBid in cardiomyocytes from WT and Mcpt4−/− mice after cells were treated with or without H2O2. F. Immunoblot analysis of CatS, CatK, CatL, and CatB in cardiomyocytes from WT and Mcpt4−/− mice after cells were treated with or without H2O2. The same blots were reprobed for β-Actin to ensure equal protein loading. Immunoblot data are representative of three independent experiments. P<0.05 was considered statistically significant, independent t-test or one-way ANOVA with post-hoc Bonferroni test. Data are mean±SEM.

    Journal: Biochimica et biophysica acta. Molecular basis of disease

    Article Title: Deficiency of mouse mast cell protease 4 mitigates cardiac dysfunctions in mice after myocardium infarction

    doi: 10.1016/j.bbadis.2019.01.011

    Figure Lengend Snippet: Role of mMCP4 in cardiomyocyte apoptosis. A/B. Representative FACS analysis and quantification of Annexin V+PI− early apoptotic cardiomyocytes and Annexin V+PI+ late apoptotic cardiomyocytes from WT and Mcpt4−/− mice after cells were treated with and without (Control) H2O2. C/D. Annexin V and PI immunofluorescent staining representative images and apoptosis quantification of cardiomyocytes from WT and Mcpt4−/− mice with and without 100 μM H2O2 treatment. Data are mean±SEM from six independent experiments. Scale: 200 μm, inset scale: 70 μm. E. Immunoblot analysis of Bax, Bid, and tBid in cardiomyocytes from WT and Mcpt4−/− mice after cells were treated with or without H2O2. F. Immunoblot analysis of CatS, CatK, CatL, and CatB in cardiomyocytes from WT and Mcpt4−/− mice after cells were treated with or without H2O2. The same blots were reprobed for β-Actin to ensure equal protein loading. Immunoblot data are representative of three independent experiments. P<0.05 was considered statistically significant, independent t-test or one-way ANOVA with post-hoc Bonferroni test. Data are mean±SEM.

    Article Snippet: Immunofluorescent, immunohistological, and Masson’s trichrome staining To localize apoptotic cells and detect the expression of mMCP4 in the heart, heart frozen sections (6 μm) were used for immunofluorescent staining for cardiomyocyte (myosin heavy chain, 1:50, Cat# bs-15444R-A488, Bioss In.

    Techniques: Staining, Western Blot

    SMS protects cardiomyocytes from apoptosis induced by diabetes. ( A ) Standard pictures of myocardial tissue sections stained with TUNEL (magnification = 630×). Scale bar 100 μm. ( B ) Ratios of TUNEL-positive cells in different groups (n = 6 rats per group). Results are presented as means ± standard deviations. ** p < 0.01 vs the NC group and ## p < 0.01 vs the DM group.

    Journal: Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy

    Article Title: ShengMai-San Attenuates Cardiac Remodeling in Diabetic Rats by Inhibiting NOX-Mediated Oxidative Stress

    doi: 10.2147/DMSO.S287582

    Figure Lengend Snippet: SMS protects cardiomyocytes from apoptosis induced by diabetes. ( A ) Standard pictures of myocardial tissue sections stained with TUNEL (magnification = 630×). Scale bar 100 μm. ( B ) Ratios of TUNEL-positive cells in different groups (n = 6 rats per group). Results are presented as means ± standard deviations. ** p < 0.01 vs the NC group and ## p < 0.01 vs the DM group.

    Article Snippet: Apoptotic cardiomyocytes were visualized by TUNEL staining according to the manufacturer’s instructions (KeyGEN Biotech, Nanjing, China).

    Techniques: Staining, TUNEL Assay