Proteinase‑activated receptor�2 deficiency is a protective factor against cardiomyocyte apoptosis during myocardial ischemia/reperfusion injury

Figures

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  Figure 1.. Efficiency of PAR2 knockdown in H9c2 cells. H9c2 cells were transfected with a PAR2 siRNA (si-PAR2) or non-specific siRNA (si-NC). (A) Knockdown efficiency evaluated by western blot analyses. (B) Densitometric analyses of the antibody-bound protein bands in the western blot analyses (*P<0.05 and **P<0.01 compared to si-NC). PAR2, proteinase-activated receptor 2.

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  Figure 2.. Result of PAR2-knockout mouse PCR amplification. PAR2 knockout mice generated a single PCR product of 198 bp. PAR2, proteinase-activated receptor 2.

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  Figure 3.. Effects of PAR2 knockout on cardiac function after MI/RI in vivo. (A) Representative echocardiographs of mice after MI/RI. (B) Percentages of LVEF and LVFS after MI/RI (*P<0.05 and **P<0.01). PAR2, proteinase-activated receptor 2; MI/RI, myocardial ischemia/reperfusion injury; LV, left ventricular; LVEF, LV ejection fraction; LVFS, LV fractional shortening.

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  Figure 4.. IA and AAR data in the LV after MI/RI. (A) Representative Evans Blue-stained images of the myocardium in PAR2+/+ mice and PAR2−/− mice. (B) Summarized data for ratios of AAR to LV, IA to LV and IA to AAR in PAR2+/+ mice and PAR2−/− mice (*P<0.05). AAR, area at risk; IA, infarct area; LV, left ventricular; MI/RI, myocardial ischemia/reperfusion injury; PAR2, proteinase-activated receptor 2.

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  Figure 5.. Apoptosis of cardiac myocytes is decreased in PAR2−/− mice after MI/RI. (A) Representative photomicrographs of TUNEL-stained myocardial sections from PAR2+/+ mice and PAR2−/− mice (×40 magnification). (B) Quantification of mean AI scores obtained in the TUNEL assays (**P<0.01). PAR2, proteinase-activated receptor 2; MI/RI, myocardial ischemia/reperfusion injury; TUNEL, terminal deoxynucleotide transferase-mediated dUTP nick end-labeling; AP, apoptosis index.

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  Figure 6.. Effects of PAR2 knockdown on percentages of apoptotic H9c2 cells. (A) After H/R treatment, H9c2 cells were stained with FITC-Annexin V and PI and evaluated by flow cytometry. (B) The percentages of Annexin V+/PI− cells were analyzed (**P<0.01). PAR2, proteinase-activated receptor 2 PI, propidium iodide; H/R, hypoxia/reoxygenation.

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  Figure 7.. Effects of PAR2 knockdown on apoptosis-associated molecules. (A) Western blot analyses of cleaved PARP and Bcl-2 in the indicated groups. (B) Densitometric analyses of the antibody-bound protein bands in the western blotting analyses (**P<0.01). PAR2, proteinase-activated receptor 2; PARP, poly-ADP-ribose polymerase; Bcl-2, B-cell lymphoma 2.

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  Figure 8.. Effects of PAR2 knockdown on MAPK signaling pathways in H9c2 cells after H/R injury. (A) Representative western blotting images for phosphorylation levels of ERK1/2, JNK, and p38 MAPK. (B) Densitometric analyses of antibody-bound protein bands in the western blot analyses (**P<0.01). PAR2, proteinase-activated receptor 2; H/R, hypoxia/reoxygenation; ERK, extracellular signal regulated kinase; JNK, c-Jun NH2-terminal protein kinase.