Fig. 2.

AK144717 knockdown suppressed the cardiac remodeling in vivo. A. qPCR analysis of AK144717 expression in NMCMs, MCMECs and NMCFs (n = 3). B. qPCR analysis of AK144717 expressions in the nucleus and cytoplasm of NMCMs. GAPDH and U6 were used as the cytoplasmic or the nuclear marker respectively (n = 4). C. The flowchart of in vivo experiment. D–E. Western blot analysis of phospho-ataxia telangiectasia mutated (Ser1981) (p-ATM)/total ATM (t-ATM) and phosphorylated histone H2AX (Ser139) (γ-H2AX) (n = 6–7). F–H. Quantitative analysis of AK144717, ANP and BNP mRNAs (n = 6). I–J. Representative images of H&E staining (upper) and WGA staining (n = 6). Scale bar: 100 μm. K. Quantitative analysis of HW/BW ratio (n = 6). L–N. Echocardiography and quantitative analysis (n = 6). O. Western blot analysis of p-/t-ATM, γ-H2AX (n = 6). *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001; NS means not significant between groups