Fig 4. MED30 deletion in adult cardiomyocyte leads to rapidly developed dilated cardiomyopathy (DCM) and lethality.

(A-B) Representative immunoblots (A) and quantification analysis (B) of MED30 in the heart isolated from inducible Med30 cardiomyocyte specific knockout (icKO) and control (Ctrl) mice at 2 weeks and 4 weeks post-tamoxifen injection. GAPDH served as a loading control. n = 3. (C) Kaplan-Meier survival curves of Med30 icKO and control and mice after oil (n = 12–16) or tamoxifen injection (n = 22–29). (D) Representative hearts (top) and H&E stained sections (bottom) of Med30 icKO and Ctrl mice at 2 weeks and 4 weeks post-tamoxifen injection. (E) Representative M-mode echocardiography of Med30 icKO and Ctrl mice at 2 weeks and 4 weeks post-tamoxifen injection. (F-I) Echocardiographic measurements for Med30 icKO and Ctrl mice at baseline, 2, 3 and 4 weeks (wks) post-tamoxifen injection by (F) fractional shortening (FS), and left ventricular (LV) internal dimensions at (G) end-diastole (LVIDd) and (H) end-systole (LVIDs), as well as LV posterior wall thickness at the end-diastolic (LVPWd). n = 14 mice per group. (J-M) qRT-PCR analysis of cardiac fetal gene markers atrial natriuretic factor (Anf) (J) and B-type natriuretic peptide (Bnp) (K), and profibrotic genes, collagen α1 types I (Col1a1) (L) and III (Col3a1) (M), in control and icKO mouse hearts at 4 weeks post-tamoxifen injection. Data were normalized to corresponding 18s levels, and icKO is expressed as the fold-change versus control. n = 3. (N-O) Representative immunostaining images (N) and quantification analysis (O) of TUNEL staining (green) in heart sections from Med30 icKO and Ctrl mice at 4 weeks post-tamoxifen injection, using an antibody against α-actinin as cardiomyocyte marker (red). DNA is stained with DAPI (blue). Scale bar: 10 μm. n = 3. Data are represented as the mean ± SEM. *P < 0.05, by 2-tailed Student’s t test, or by the Kaplan-Meier survival analysis.