Fig. 5

CaMKII inhibition by KN93 treatment prevents against pathological responses triggered by PRMT1 depletion. a CaMKII protein analysis of control or PRMT1-depleted NRVM cells treated with vehicle or KN93 for 24 h. b Representative images for NRVM cells immunostained with indicated antibodies. Scale bar: 50 μm. c Quantification of surface area of cells from similar experiments shown in b. n = 82 (Ad-shscr); n = 75 (Ad-shPRMT1); n = 78 (KN93-treated Ad-shPRMT1). Data represent means ± SD. ^***P < 0.001, Student’s t-test. d qRT-PCR analysis of ANP, and β-MHC levels in control and PRMT1-depleted NRVM cells treated with vehicle or KN93. Data represent means ± SD. ^*P < 0.05, ^**P < 0.01, ^***P < 0.001, Student’s t-test. e Representative AP traces in ventricular myocytes stimulated at 2 Hz from f/f and cKO mice. f Summary of the time required for 90% repolarization (APD90) showed that AP from cKO mice is dramatically prolonged. The APs were recorded from 7-weeks-old mice. n = 5. Data represent means ± SD. ^*P < 0.05, ^**P < 0.01, Student’s t-test. g–h Representative AP traces in ventricular myocytes stimulated at 0.5 Hz from cKO in the presence and absence of KN93 (g) or KN92 (h). i Bar graph showing the average APD90 of ventricular myocytes stimulated at 0.5 Hz from cKO mice in the absence and presence of KN93 or KN92. Data represent means ± SEM. **P < 0.01, Student’s t-test