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. 2017 Oct 28;6(11):e007030. doi: 10.1161/JAHA.117.007030

Figure 6.

Figure 6

Acute MYL4 p.E11K gene transfer causes NRCM apoptosis and activates profibrotic signaling. A through C, Western blot and quantitative RT‐PCR analysis of MYL4 expression in NRCM exposed to gene transfer with different adenoviral constructs. D and E, Cardiomyocytes exposed to MYL4 E11K adenovirus showed significantly greater TUNEL‐positivity compared with WT. TUNEL‐positive staining is FITC (green). Nuclei are stained with DAPI (blue). Myocytes are stained for α‐actin (red). Arrows indicate TUNEL‐positive nuclei. F through K, Western blot analysis for proapoptotic protein caspase‐3 and antiapoptotic protein Bcl‐2 (F through I) and Smad/JNK signaling. Data are mean±SEM. The sample sizes were N=3 NRCM isolations per group with n=3 replicates from each isolate for each experiment. *P<0.05. Bax indicates B‐cell lymphoma 2–associated X protein; Bcl‐2, B‐cell lymphoma 2; Ctr indicates control; DAPI, 4′,6‐diamidino‐2‐phenylindole; JNK, c‐Jun N‐terminal kinase; MYL4, myosin light‐chain 4; N, number; NRCM, neonatal rat cardiomyocytes; Smad, small mothers against decapentaplegic; TUNEL, terminal deoxynucleotidyl transferase dUTP nick end labeling; WT, wild type.