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. 2013 Apr 8;210(4):665–673. doi: 10.1084/jem.20122126

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© 2013 Takefuji et al.

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Figure 4. — Cardiomyocyte-specific inactivation of RhoGEF12 improves cardiac function and survival in preexisting hypertrophy. (A) Experimental design. (B–E) Control mice (blue lines, diamonds) and not yet induced cmc-GEF12-KOs (red lines, squares) were subjected to sham surgery (dashed lines) or TAC (solid lines) at day 0, followed by tamoxifen (Tam) induction of recombination on days 14–18. MRI analysis of left ventricular end-diastolic (LVED) wall thickness (B), left ventricular (LV) ejection fraction (C), and LVED volume (D, exemplary MRI images; E, statistical evaluation) was performed before and 2, 6, 14, 25, and 52 wk after surgery (n = 15). (F) Survival plot for control and cmc-GEF12-KOs up to 1 yr after TAC, followed by tamoxifen injection (n = 18–24). (G) RhoA activation in adult hearts from control mice and cmc-GEF12-KOs 1 yr after TAC (n = 3). (H) TAC-induced fibrosis 1 yr after TAC as determined by Picrosirius red staining (n = 5). (I) Expression of ANP and BNP 1 yr after sham surgery or TAC as determined by qRT-PCR in whole hearts (n = 3–5; data normalized to GAPDH, control values set to 1). (J) Apoptosis was determined by TUNEL staining in left ventricles 1 yr after TAC (n = 3). Error bars indicate SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001.