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Signalway Antibody anti cleaved caspase 3
CRTH 2 deletion reduces doxorubicin‐induced cardiomyocyte apoptosis and cardiac injury in mice Western blot analysis of ER stress markers p‐IRE1 and cleaved ATF6 in mouse cardiomyocytes upon DOX (1 μmol/l) treatment. CRTH2 mRNA expression in mouse cardiomyocytes under DOX treatment. Data represent mean ± SEM. ** P = 0.00011, 12 h vs. 0 h; ** P = 0.000267, 24 h vs. 0 h (one‐way ANOVA); n = 4. Cardiac function in mice assessed by M‐mode echocardiographic analysis on day 7 after DOX treatment (20 mg/kg, i.p.). EF, ejection fraction (C); FS, fractional shortening (D); LVPWs, left ventricle posterior wall thickness at end‐systole (E). Data represent mean ± SEM. EF, * P = 0.00836, vs. WT; FS, * P = 0.00383, vs. WT; LVPWs, * P = 0.0198, vs. WT (unpaired two‐tailed t ‐test); WT, n = 15, CRTH2 −/− , n = 13. Kaplan–Meier survival curves for mice subjected to DOX treatment. * P = 0.0305, vs. WT (log‐rank test); n = 15. Representative TUNEL‐stained images of heart tissue in mice on day 7 after DOX treatment. Green, TUNEL‐positive nuclei; blue, DAPI; red, α‐actinin; scale bar, 50 μm. Quantification of TUNEL‐positive cardiomyocytes in (G). Data represent mean ± SEM. * P = 0.00278, vs. WT (unpaired two‐tailed t ‐test); n = 6. Western blot analysis of m‐calpain, caspase‐12, and <t>caspase‐3</t> in heart tissue from DOX‐treated mice. Schematic diagram of CRTH2 promoting cardiomyocyte apoptosis under ER stress through the G αq /calpain/caspase‐12 signaling pathway. Source data are available online for this figure.
Anti Cleaved Caspase 3, supplied by Signalway Antibody, used in various techniques. Bioz Stars score: 92/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti cleaved caspase 3/product/Signalway Antibody
Average 92 stars, based on 3 article reviews
Price from $9.99 to $1999.99
anti cleaved caspase 3 - by Bioz Stars, 2020-09
92/100 stars

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1) Product Images from "CRTH2 promotes endoplasmic reticulum stress‐induced cardiomyocyte apoptosis through m‐calpain"

Article Title: CRTH2 promotes endoplasmic reticulum stress‐induced cardiomyocyte apoptosis through m‐calpain

Journal: EMBO Molecular Medicine

doi: 10.15252/emmm.201708237

CRTH 2 deletion reduces doxorubicin‐induced cardiomyocyte apoptosis and cardiac injury in mice Western blot analysis of ER stress markers p‐IRE1 and cleaved ATF6 in mouse cardiomyocytes upon DOX (1 μmol/l) treatment. CRTH2 mRNA expression in mouse cardiomyocytes under DOX treatment. Data represent mean ± SEM. ** P = 0.00011, 12 h vs. 0 h; ** P = 0.000267, 24 h vs. 0 h (one‐way ANOVA); n = 4. Cardiac function in mice assessed by M‐mode echocardiographic analysis on day 7 after DOX treatment (20 mg/kg, i.p.). EF, ejection fraction (C); FS, fractional shortening (D); LVPWs, left ventricle posterior wall thickness at end‐systole (E). Data represent mean ± SEM. EF, * P = 0.00836, vs. WT; FS, * P = 0.00383, vs. WT; LVPWs, * P = 0.0198, vs. WT (unpaired two‐tailed t ‐test); WT, n = 15, CRTH2 −/− , n = 13. Kaplan–Meier survival curves for mice subjected to DOX treatment. * P = 0.0305, vs. WT (log‐rank test); n = 15. Representative TUNEL‐stained images of heart tissue in mice on day 7 after DOX treatment. Green, TUNEL‐positive nuclei; blue, DAPI; red, α‐actinin; scale bar, 50 μm. Quantification of TUNEL‐positive cardiomyocytes in (G). Data represent mean ± SEM. * P = 0.00278, vs. WT (unpaired two‐tailed t ‐test); n = 6. Western blot analysis of m‐calpain, caspase‐12, and caspase‐3 in heart tissue from DOX‐treated mice. Schematic diagram of CRTH2 promoting cardiomyocyte apoptosis under ER stress through the G αq /calpain/caspase‐12 signaling pathway. Source data are available online for this figure.
Figure Legend Snippet: CRTH 2 deletion reduces doxorubicin‐induced cardiomyocyte apoptosis and cardiac injury in mice Western blot analysis of ER stress markers p‐IRE1 and cleaved ATF6 in mouse cardiomyocytes upon DOX (1 μmol/l) treatment. CRTH2 mRNA expression in mouse cardiomyocytes under DOX treatment. Data represent mean ± SEM. ** P = 0.00011, 12 h vs. 0 h; ** P = 0.000267, 24 h vs. 0 h (one‐way ANOVA); n = 4. Cardiac function in mice assessed by M‐mode echocardiographic analysis on day 7 after DOX treatment (20 mg/kg, i.p.). EF, ejection fraction (C); FS, fractional shortening (D); LVPWs, left ventricle posterior wall thickness at end‐systole (E). Data represent mean ± SEM. EF, * P = 0.00836, vs. WT; FS, * P = 0.00383, vs. WT; LVPWs, * P = 0.0198, vs. WT (unpaired two‐tailed t ‐test); WT, n = 15, CRTH2 −/− , n = 13. Kaplan–Meier survival curves for mice subjected to DOX treatment. * P = 0.0305, vs. WT (log‐rank test); n = 15. Representative TUNEL‐stained images of heart tissue in mice on day 7 after DOX treatment. Green, TUNEL‐positive nuclei; blue, DAPI; red, α‐actinin; scale bar, 50 μm. Quantification of TUNEL‐positive cardiomyocytes in (G). Data represent mean ± SEM. * P = 0.00278, vs. WT (unpaired two‐tailed t ‐test); n = 6. Western blot analysis of m‐calpain, caspase‐12, and caspase‐3 in heart tissue from DOX‐treated mice. Schematic diagram of CRTH2 promoting cardiomyocyte apoptosis under ER stress through the G αq /calpain/caspase‐12 signaling pathway. Source data are available online for this figure.

Techniques Used: Mouse Assay, Western Blot, Expressing, Two Tailed Test, TUNEL Assay, Staining

CRTH 2 inhibition protects against myocardial infarction ( MI ) by reducing ischemia‐induced apoptosis in mice Representative TUNEL‐stained images of the peri‐infarct area in MI mouse heart. Green, TUNEL‐positive nuclei; blue, DAPI; red, α‐actinin; scale bar, 50 μm. Quantification of TUNEL‐positive cardiomyocytes. Data represent mean ± SEM. * P = 0.0147, vs. WT (unpaired two‐tailed t ‐test); WT, n = 6; CRTH2 −/− , n = 8. Western blot analysis of the activated caspase‐3 in the infarct border zone of mouse heart post‐MI. M‐mode echocardiographic analysis of cardiac function in mice at day 14 post‐MI. EF, ejection fraction (D); FS, fractional shortening (E); LVPWs, left ventricular posterior wall thickness at end‐systole. (F). Data represent mean ± SEM. EF, * P = 0.0015, vs. WT (unpaired two‐tailed t ‐test); FS, * P = 0.0015, vs. WT (unpaired two‐tailed t ‐test); LVPWs, * P = 0.00805, vs. WT (unpaired two‐tailed t ‐test); WT, n = 10; CRTH2 −/− , n = 12. Representative images of Evans blue and TTC‐stained mouse heart at day 14 post‐MI. Scale bar, 500 μm. Quantification of infarcted size in mouse heart after MI. Data represent mean ± SEM. ** P = 0.00354, vs. WT (unpaired two‐tailed t ‐test); n = 10. Heart weight‐to‐body weight ratio in mice subjected to MI. Data represent mean ± SEM. * P = 0.0119, vs. WT (unpaired two‐tailed t ‐test); WT and CRTH2 −/− (Sham), n = 8; WT and CRTH2 −/− (MI), n = 10. Kaplan–Meier survival curves for mice at day 14 post‐MI. * P = 0.0356, vs. WT (log‐rank test).WT, n = 29; CRTH2 −/− , n = 26. Representative images of Masson's trichrome staining of cardiac tissues from infarcted hearts. Scale bar, 20 μm. Quantification of collagen content in (K). Data represent mean ± SEM. * P = 0.0196, vs. WT (unpaired two‐tailed t ‐test); WT and CRTH2 −/− (Sham), n = 7; WT and CRTH2 −/− (MI), n = 9. Source data are available online for this figure.
Figure Legend Snippet: CRTH 2 inhibition protects against myocardial infarction ( MI ) by reducing ischemia‐induced apoptosis in mice Representative TUNEL‐stained images of the peri‐infarct area in MI mouse heart. Green, TUNEL‐positive nuclei; blue, DAPI; red, α‐actinin; scale bar, 50 μm. Quantification of TUNEL‐positive cardiomyocytes. Data represent mean ± SEM. * P = 0.0147, vs. WT (unpaired two‐tailed t ‐test); WT, n = 6; CRTH2 −/− , n = 8. Western blot analysis of the activated caspase‐3 in the infarct border zone of mouse heart post‐MI. M‐mode echocardiographic analysis of cardiac function in mice at day 14 post‐MI. EF, ejection fraction (D); FS, fractional shortening (E); LVPWs, left ventricular posterior wall thickness at end‐systole. (F). Data represent mean ± SEM. EF, * P = 0.0015, vs. WT (unpaired two‐tailed t ‐test); FS, * P = 0.0015, vs. WT (unpaired two‐tailed t ‐test); LVPWs, * P = 0.00805, vs. WT (unpaired two‐tailed t ‐test); WT, n = 10; CRTH2 −/− , n = 12. Representative images of Evans blue and TTC‐stained mouse heart at day 14 post‐MI. Scale bar, 500 μm. Quantification of infarcted size in mouse heart after MI. Data represent mean ± SEM. ** P = 0.00354, vs. WT (unpaired two‐tailed t ‐test); n = 10. Heart weight‐to‐body weight ratio in mice subjected to MI. Data represent mean ± SEM. * P = 0.0119, vs. WT (unpaired two‐tailed t ‐test); WT and CRTH2 −/− (Sham), n = 8; WT and CRTH2 −/− (MI), n = 10. Kaplan–Meier survival curves for mice at day 14 post‐MI. * P = 0.0356, vs. WT (log‐rank test).WT, n = 29; CRTH2 −/− , n = 26. Representative images of Masson's trichrome staining of cardiac tissues from infarcted hearts. Scale bar, 20 μm. Quantification of collagen content in (K). Data represent mean ± SEM. * P = 0.0196, vs. WT (unpaired two‐tailed t ‐test); WT and CRTH2 −/− (Sham), n = 7; WT and CRTH2 −/− (MI), n = 9. Source data are available online for this figure.

Techniques Used: Inhibition, Mouse Assay, TUNEL Assay, Staining, Two Tailed Test, Western Blot

CRTH 2 deletion attenuates anoxia‐induced cardiomyocyte apoptosis in vitro Representative TUNEL‐stained images of mouse cardiomyocytes challenged with anoxia. Green, TUNEL‐positive nuclei; blue, DAPI‐stained nuclei; red, cardiomyocytes labeled with antibody to α‐actinin; scale bar, 50 μm. Quantification of TUNEL‐positive cells in (A). Data represent mean ± SEM. **P = 0.00202, vs. WT (Mann–Whitney U ‐test); n = 6. Flow cytometry analysis of annexin V and propidium iodide (PI) staining of apoptotic cardiomyocytes following anoxia treatment. Quantification of annexin V + cells in (C). Data represent mean ± SEM. * P = 0.0002, vs. WT (unpaired two‐tailed t ‐test); n = 6. Western blot analysis of activated caspase‐3 in mouse cardiomyocytes challenged with anoxia. Source data are available online for this figure.
Figure Legend Snippet: CRTH 2 deletion attenuates anoxia‐induced cardiomyocyte apoptosis in vitro Representative TUNEL‐stained images of mouse cardiomyocytes challenged with anoxia. Green, TUNEL‐positive nuclei; blue, DAPI‐stained nuclei; red, cardiomyocytes labeled with antibody to α‐actinin; scale bar, 50 μm. Quantification of TUNEL‐positive cells in (A). Data represent mean ± SEM. **P = 0.00202, vs. WT (Mann–Whitney U ‐test); n = 6. Flow cytometry analysis of annexin V and propidium iodide (PI) staining of apoptotic cardiomyocytes following anoxia treatment. Quantification of annexin V + cells in (C). Data represent mean ± SEM. * P = 0.0002, vs. WT (unpaired two‐tailed t ‐test); n = 6. Western blot analysis of activated caspase‐3 in mouse cardiomyocytes challenged with anoxia. Source data are available online for this figure.

Techniques Used: In Vitro, TUNEL Assay, Staining, Labeling, MANN-WHITNEY, Flow Cytometry, Cytometry, Two Tailed Test, Western Blot

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Article Title: PIWI-Interacting RNA-004800 Is Regulated by S1P Receptor Signaling Pathway to Keep Myeloma Cell Survival
Article Snippet: Antibodies and Reagents Anti-Mcl-1 (1:1,000), anti-BAD (1:500), anti-Bcl-2 (1:1,000), anti-Bcl-XL (1:500), anti-cleaved caspase-3 (1:500), anti-Stat3 (1:1,000), anti-LC3B (1:1,500), anti-beclin1 (1:1,000), and anti-β-actin (1:1,000) antibodies were purchased from Signalway antibody (College Park, Maryland, USA).

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    Signalway Antibody anti cleaved caspase 3
    CRTH 2 deletion reduces doxorubicin‐induced cardiomyocyte apoptosis and cardiac injury in mice Western blot analysis of ER stress markers p‐IRE1 and cleaved ATF6 in mouse cardiomyocytes upon DOX (1 μmol/l) treatment. CRTH2 mRNA expression in mouse cardiomyocytes under DOX treatment. Data represent mean ± SEM. ** P = 0.00011, 12 h vs. 0 h; ** P = 0.000267, 24 h vs. 0 h (one‐way ANOVA); n = 4. Cardiac function in mice assessed by M‐mode echocardiographic analysis on day 7 after DOX treatment (20 mg/kg, i.p.). EF, ejection fraction (C); FS, fractional shortening (D); LVPWs, left ventricle posterior wall thickness at end‐systole (E). Data represent mean ± SEM. EF, * P = 0.00836, vs. WT; FS, * P = 0.00383, vs. WT; LVPWs, * P = 0.0198, vs. WT (unpaired two‐tailed t ‐test); WT, n = 15, CRTH2 −/− , n = 13. Kaplan–Meier survival curves for mice subjected to DOX treatment. * P = 0.0305, vs. WT (log‐rank test); n = 15. Representative TUNEL‐stained images of heart tissue in mice on day 7 after DOX treatment. Green, TUNEL‐positive nuclei; blue, DAPI; red, α‐actinin; scale bar, 50 μm. Quantification of TUNEL‐positive cardiomyocytes in (G). Data represent mean ± SEM. * P = 0.00278, vs. WT (unpaired two‐tailed t ‐test); n = 6. Western blot analysis of m‐calpain, caspase‐12, and <t>caspase‐3</t> in heart tissue from DOX‐treated mice. Schematic diagram of CRTH2 promoting cardiomyocyte apoptosis under ER stress through the G αq /calpain/caspase‐12 signaling pathway. Source data are available online for this figure.
    Anti Cleaved Caspase 3, supplied by Signalway Antibody, used in various techniques. Bioz Stars score: 92/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti cleaved caspase 3/product/Signalway Antibody
    Average 92 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    anti cleaved caspase 3 - by Bioz Stars, 2020-09
    92/100 stars
      Buy from Supplier

    90
    Signalway Antibody rabbit anti cleaved caspase 3 polyclonal antibody
    CRTH 2 deletion reduces doxorubicin‐induced cardiomyocyte apoptosis and cardiac injury in mice Western blot analysis of ER stress markers p‐IRE1 and cleaved ATF6 in mouse cardiomyocytes upon DOX (1 μmol/l) treatment. CRTH2 mRNA expression in mouse cardiomyocytes under DOX treatment. Data represent mean ± SEM. ** P = 0.00011, 12 h vs. 0 h; ** P = 0.000267, 24 h vs. 0 h (one‐way ANOVA); n = 4. Cardiac function in mice assessed by M‐mode echocardiographic analysis on day 7 after DOX treatment (20 mg/kg, i.p.). EF, ejection fraction (C); FS, fractional shortening (D); LVPWs, left ventricle posterior wall thickness at end‐systole (E). Data represent mean ± SEM. EF, * P = 0.00836, vs. WT; FS, * P = 0.00383, vs. WT; LVPWs, * P = 0.0198, vs. WT (unpaired two‐tailed t ‐test); WT, n = 15, CRTH2 −/− , n = 13. Kaplan–Meier survival curves for mice subjected to DOX treatment. * P = 0.0305, vs. WT (log‐rank test); n = 15. Representative TUNEL‐stained images of heart tissue in mice on day 7 after DOX treatment. Green, TUNEL‐positive nuclei; blue, DAPI; red, α‐actinin; scale bar, 50 μm. Quantification of TUNEL‐positive cardiomyocytes in (G). Data represent mean ± SEM. * P = 0.00278, vs. WT (unpaired two‐tailed t ‐test); n = 6. Western blot analysis of m‐calpain, caspase‐12, and <t>caspase‐3</t> in heart tissue from DOX‐treated mice. Schematic diagram of CRTH2 promoting cardiomyocyte apoptosis under ER stress through the G αq /calpain/caspase‐12 signaling pathway. Source data are available online for this figure.
    Rabbit Anti Cleaved Caspase 3 Polyclonal Antibody, supplied by Signalway Antibody, 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 cleaved caspase 3 polyclonal antibody/product/Signalway Antibody
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti cleaved caspase 3 polyclonal antibody - by Bioz Stars, 2020-09
    90/100 stars
      Buy from Supplier

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    CRTH 2 deletion reduces doxorubicin‐induced cardiomyocyte apoptosis and cardiac injury in mice Western blot analysis of ER stress markers p‐IRE1 and cleaved ATF6 in mouse cardiomyocytes upon DOX (1 μmol/l) treatment. CRTH2 mRNA expression in mouse cardiomyocytes under DOX treatment. Data represent mean ± SEM. ** P = 0.00011, 12 h vs. 0 h; ** P = 0.000267, 24 h vs. 0 h (one‐way ANOVA); n = 4. Cardiac function in mice assessed by M‐mode echocardiographic analysis on day 7 after DOX treatment (20 mg/kg, i.p.). EF, ejection fraction (C); FS, fractional shortening (D); LVPWs, left ventricle posterior wall thickness at end‐systole (E). Data represent mean ± SEM. EF, * P = 0.00836, vs. WT; FS, * P = 0.00383, vs. WT; LVPWs, * P = 0.0198, vs. WT (unpaired two‐tailed t ‐test); WT, n = 15, CRTH2 −/− , n = 13. Kaplan–Meier survival curves for mice subjected to DOX treatment. * P = 0.0305, vs. WT (log‐rank test); n = 15. Representative TUNEL‐stained images of heart tissue in mice on day 7 after DOX treatment. Green, TUNEL‐positive nuclei; blue, DAPI; red, α‐actinin; scale bar, 50 μm. Quantification of TUNEL‐positive cardiomyocytes in (G). Data represent mean ± SEM. * P = 0.00278, vs. WT (unpaired two‐tailed t ‐test); n = 6. Western blot analysis of m‐calpain, caspase‐12, and caspase‐3 in heart tissue from DOX‐treated mice. Schematic diagram of CRTH2 promoting cardiomyocyte apoptosis under ER stress through the G αq /calpain/caspase‐12 signaling pathway. Source data are available online for this figure.

    Journal: EMBO Molecular Medicine

    Article Title: CRTH2 promotes endoplasmic reticulum stress‐induced cardiomyocyte apoptosis through m‐calpain

    doi: 10.15252/emmm.201708237

    Figure Lengend Snippet: CRTH 2 deletion reduces doxorubicin‐induced cardiomyocyte apoptosis and cardiac injury in mice Western blot analysis of ER stress markers p‐IRE1 and cleaved ATF6 in mouse cardiomyocytes upon DOX (1 μmol/l) treatment. CRTH2 mRNA expression in mouse cardiomyocytes under DOX treatment. Data represent mean ± SEM. ** P = 0.00011, 12 h vs. 0 h; ** P = 0.000267, 24 h vs. 0 h (one‐way ANOVA); n = 4. Cardiac function in mice assessed by M‐mode echocardiographic analysis on day 7 after DOX treatment (20 mg/kg, i.p.). EF, ejection fraction (C); FS, fractional shortening (D); LVPWs, left ventricle posterior wall thickness at end‐systole (E). Data represent mean ± SEM. EF, * P = 0.00836, vs. WT; FS, * P = 0.00383, vs. WT; LVPWs, * P = 0.0198, vs. WT (unpaired two‐tailed t ‐test); WT, n = 15, CRTH2 −/− , n = 13. Kaplan–Meier survival curves for mice subjected to DOX treatment. * P = 0.0305, vs. WT (log‐rank test); n = 15. Representative TUNEL‐stained images of heart tissue in mice on day 7 after DOX treatment. Green, TUNEL‐positive nuclei; blue, DAPI; red, α‐actinin; scale bar, 50 μm. Quantification of TUNEL‐positive cardiomyocytes in (G). Data represent mean ± SEM. * P = 0.00278, vs. WT (unpaired two‐tailed t ‐test); n = 6. Western blot analysis of m‐calpain, caspase‐12, and caspase‐3 in heart tissue from DOX‐treated mice. Schematic diagram of CRTH2 promoting cardiomyocyte apoptosis under ER stress through the G αq /calpain/caspase‐12 signaling pathway. Source data are available online for this figure.

    Article Snippet: Primary antibodies were diluted as follows: anti‐cleaved‐caspase‐3 (1:1,000; Signalway Antibody LLC), anti‐mouse GAPDH, anti‐HA‐tag, anti‐m‐calpain, anti‐μ‐calpain, anti‐caspase‐12, anti‐IRE1 (1:1,000; Cell Signaling Technology), anti‐calpain‐7 (1:1,000; ProteinTech Group, Chicago, IL, USA), anti‐P‐IRE1(1:1,000; Littleton, CO, USA), anti‐ATF6 (1:500, Santa Cruz, CA, USA), anti‐LC3A/B, anti‐phospho‐MLKL, anti‐MLKL (1:1,000; Cell Signaling Technology), anti‐caspase‐4, anti‐caspase‐8, and anti‐caspase‐9 (1:1,000; ABclonal).

    Techniques: Mouse Assay, Western Blot, Expressing, Two Tailed Test, TUNEL Assay, Staining

    CRTH 2 inhibition protects against myocardial infarction ( MI ) by reducing ischemia‐induced apoptosis in mice Representative TUNEL‐stained images of the peri‐infarct area in MI mouse heart. Green, TUNEL‐positive nuclei; blue, DAPI; red, α‐actinin; scale bar, 50 μm. Quantification of TUNEL‐positive cardiomyocytes. Data represent mean ± SEM. * P = 0.0147, vs. WT (unpaired two‐tailed t ‐test); WT, n = 6; CRTH2 −/− , n = 8. Western blot analysis of the activated caspase‐3 in the infarct border zone of mouse heart post‐MI. M‐mode echocardiographic analysis of cardiac function in mice at day 14 post‐MI. EF, ejection fraction (D); FS, fractional shortening (E); LVPWs, left ventricular posterior wall thickness at end‐systole. (F). Data represent mean ± SEM. EF, * P = 0.0015, vs. WT (unpaired two‐tailed t ‐test); FS, * P = 0.0015, vs. WT (unpaired two‐tailed t ‐test); LVPWs, * P = 0.00805, vs. WT (unpaired two‐tailed t ‐test); WT, n = 10; CRTH2 −/− , n = 12. Representative images of Evans blue and TTC‐stained mouse heart at day 14 post‐MI. Scale bar, 500 μm. Quantification of infarcted size in mouse heart after MI. Data represent mean ± SEM. ** P = 0.00354, vs. WT (unpaired two‐tailed t ‐test); n = 10. Heart weight‐to‐body weight ratio in mice subjected to MI. Data represent mean ± SEM. * P = 0.0119, vs. WT (unpaired two‐tailed t ‐test); WT and CRTH2 −/− (Sham), n = 8; WT and CRTH2 −/− (MI), n = 10. Kaplan–Meier survival curves for mice at day 14 post‐MI. * P = 0.0356, vs. WT (log‐rank test).WT, n = 29; CRTH2 −/− , n = 26. Representative images of Masson's trichrome staining of cardiac tissues from infarcted hearts. Scale bar, 20 μm. Quantification of collagen content in (K). Data represent mean ± SEM. * P = 0.0196, vs. WT (unpaired two‐tailed t ‐test); WT and CRTH2 −/− (Sham), n = 7; WT and CRTH2 −/− (MI), n = 9. Source data are available online for this figure.

    Journal: EMBO Molecular Medicine

    Article Title: CRTH2 promotes endoplasmic reticulum stress‐induced cardiomyocyte apoptosis through m‐calpain

    doi: 10.15252/emmm.201708237

    Figure Lengend Snippet: CRTH 2 inhibition protects against myocardial infarction ( MI ) by reducing ischemia‐induced apoptosis in mice Representative TUNEL‐stained images of the peri‐infarct area in MI mouse heart. Green, TUNEL‐positive nuclei; blue, DAPI; red, α‐actinin; scale bar, 50 μm. Quantification of TUNEL‐positive cardiomyocytes. Data represent mean ± SEM. * P = 0.0147, vs. WT (unpaired two‐tailed t ‐test); WT, n = 6; CRTH2 −/− , n = 8. Western blot analysis of the activated caspase‐3 in the infarct border zone of mouse heart post‐MI. M‐mode echocardiographic analysis of cardiac function in mice at day 14 post‐MI. EF, ejection fraction (D); FS, fractional shortening (E); LVPWs, left ventricular posterior wall thickness at end‐systole. (F). Data represent mean ± SEM. EF, * P = 0.0015, vs. WT (unpaired two‐tailed t ‐test); FS, * P = 0.0015, vs. WT (unpaired two‐tailed t ‐test); LVPWs, * P = 0.00805, vs. WT (unpaired two‐tailed t ‐test); WT, n = 10; CRTH2 −/− , n = 12. Representative images of Evans blue and TTC‐stained mouse heart at day 14 post‐MI. Scale bar, 500 μm. Quantification of infarcted size in mouse heart after MI. Data represent mean ± SEM. ** P = 0.00354, vs. WT (unpaired two‐tailed t ‐test); n = 10. Heart weight‐to‐body weight ratio in mice subjected to MI. Data represent mean ± SEM. * P = 0.0119, vs. WT (unpaired two‐tailed t ‐test); WT and CRTH2 −/− (Sham), n = 8; WT and CRTH2 −/− (MI), n = 10. Kaplan–Meier survival curves for mice at day 14 post‐MI. * P = 0.0356, vs. WT (log‐rank test).WT, n = 29; CRTH2 −/− , n = 26. Representative images of Masson's trichrome staining of cardiac tissues from infarcted hearts. Scale bar, 20 μm. Quantification of collagen content in (K). Data represent mean ± SEM. * P = 0.0196, vs. WT (unpaired two‐tailed t ‐test); WT and CRTH2 −/− (Sham), n = 7; WT and CRTH2 −/− (MI), n = 9. Source data are available online for this figure.

    Article Snippet: Primary antibodies were diluted as follows: anti‐cleaved‐caspase‐3 (1:1,000; Signalway Antibody LLC), anti‐mouse GAPDH, anti‐HA‐tag, anti‐m‐calpain, anti‐μ‐calpain, anti‐caspase‐12, anti‐IRE1 (1:1,000; Cell Signaling Technology), anti‐calpain‐7 (1:1,000; ProteinTech Group, Chicago, IL, USA), anti‐P‐IRE1(1:1,000; Littleton, CO, USA), anti‐ATF6 (1:500, Santa Cruz, CA, USA), anti‐LC3A/B, anti‐phospho‐MLKL, anti‐MLKL (1:1,000; Cell Signaling Technology), anti‐caspase‐4, anti‐caspase‐8, and anti‐caspase‐9 (1:1,000; ABclonal).

    Techniques: Inhibition, Mouse Assay, TUNEL Assay, Staining, Two Tailed Test, Western Blot

    CRTH 2 deletion attenuates anoxia‐induced cardiomyocyte apoptosis in vitro Representative TUNEL‐stained images of mouse cardiomyocytes challenged with anoxia. Green, TUNEL‐positive nuclei; blue, DAPI‐stained nuclei; red, cardiomyocytes labeled with antibody to α‐actinin; scale bar, 50 μm. Quantification of TUNEL‐positive cells in (A). Data represent mean ± SEM. **P = 0.00202, vs. WT (Mann–Whitney U ‐test); n = 6. Flow cytometry analysis of annexin V and propidium iodide (PI) staining of apoptotic cardiomyocytes following anoxia treatment. Quantification of annexin V + cells in (C). Data represent mean ± SEM. * P = 0.0002, vs. WT (unpaired two‐tailed t ‐test); n = 6. Western blot analysis of activated caspase‐3 in mouse cardiomyocytes challenged with anoxia. Source data are available online for this figure.

    Journal: EMBO Molecular Medicine

    Article Title: CRTH2 promotes endoplasmic reticulum stress‐induced cardiomyocyte apoptosis through m‐calpain

    doi: 10.15252/emmm.201708237

    Figure Lengend Snippet: CRTH 2 deletion attenuates anoxia‐induced cardiomyocyte apoptosis in vitro Representative TUNEL‐stained images of mouse cardiomyocytes challenged with anoxia. Green, TUNEL‐positive nuclei; blue, DAPI‐stained nuclei; red, cardiomyocytes labeled with antibody to α‐actinin; scale bar, 50 μm. Quantification of TUNEL‐positive cells in (A). Data represent mean ± SEM. **P = 0.00202, vs. WT (Mann–Whitney U ‐test); n = 6. Flow cytometry analysis of annexin V and propidium iodide (PI) staining of apoptotic cardiomyocytes following anoxia treatment. Quantification of annexin V + cells in (C). Data represent mean ± SEM. * P = 0.0002, vs. WT (unpaired two‐tailed t ‐test); n = 6. Western blot analysis of activated caspase‐3 in mouse cardiomyocytes challenged with anoxia. Source data are available online for this figure.

    Article Snippet: Primary antibodies were diluted as follows: anti‐cleaved‐caspase‐3 (1:1,000; Signalway Antibody LLC), anti‐mouse GAPDH, anti‐HA‐tag, anti‐m‐calpain, anti‐μ‐calpain, anti‐caspase‐12, anti‐IRE1 (1:1,000; Cell Signaling Technology), anti‐calpain‐7 (1:1,000; ProteinTech Group, Chicago, IL, USA), anti‐P‐IRE1(1:1,000; Littleton, CO, USA), anti‐ATF6 (1:500, Santa Cruz, CA, USA), anti‐LC3A/B, anti‐phospho‐MLKL, anti‐MLKL (1:1,000; Cell Signaling Technology), anti‐caspase‐4, anti‐caspase‐8, and anti‐caspase‐9 (1:1,000; ABclonal).

    Techniques: In Vitro, TUNEL Assay, Staining, Labeling, MANN-WHITNEY, Flow Cytometry, Cytometry, Two Tailed Test, Western Blot