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. Author manuscript; available in PMC: 2017 Mar 1.
Published in final edited form as: J Mol Cell Cardiol. 2015 Nov 28;90:21–29. doi: 10.1016/j.yjmcc.2015.11.030

Fig. 6. PAR4 stimulation mediates cardiomyocyte apoptosis.

Fig. 6

(A–B) Neonatal rat cardiac myocytes were transduced with adenoviruses expressing shRNA PAR4 (Ad-shCbl, 10 pfu/cell) or shRNA control (Ad-shCtrl, 10 pfu/cell) for 48 h and then untreated or treated with 1 or 10 U/ml thrombin (Thr), 500 μM PAR4-AP (AYPGKF) or 300 μM PAR1/PAR2-AP (SFLLRN) for 24 h. Caspase-3 activity (A) and the percent of TUNEL-positive nuclei (B) were assayed in triplicate. (C–D) Lysates from myocytes infected with Ad-shCtrl, Ad-shPAR4 (C), Lac.Z (10 pfu/cell) or WT-PAR4 (D) adenoviruses for 48 h were assessed for immunoblot analysis. (E–F) Myocytes infected with Lac.Z or WT-PAR4 adenoviruses were treated with the indicated agonists for 24 h and assayed for caspase-3 activity (E) or TUNEL assay (F). Results are representative of 3 independent experiments. Data are mean ± SEM; *P<0.05 vs. control; †P<0.05 vs. treated myocytes.