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. 2017 Jan 4;292(6):2345–2358. doi: 10.1074/jbc.M116.764522

FIGURE 5.

FIGURE 5.

Conditional, cardiomyocyte-specific Traf3ip2 gene deletion attenuates I/R-induced adverse myocardial remodeling. A, Traf3ip2 gene deletion blunts progression of I/R-contractile dysfunction and progression to heart failure. Following 30 min ischemia and reperfusion for up 12 weeks, myocardial function was analyzed by echocardiography. LVIDs, Left ventricular internal dimension at end-systole; LV Vol, LV volume; LVPWs, left ventricular posterior wall thickness at end-systole. *, p < at least 0.05 versus control-I/R (n = 5 = 6/group). B, Traf3ip2 gene deletion attenuates development of hypertrophy in the non-ischemic zone. Cardiomyocyte cross-sectional area after a 12-week reperfusion was analyzed in H&E-stained sections by ImageJ software. Although representative images are shown on the left, the mean area was quantified and summarized on the right. *, p < 0.001 versus control-I/R (n = 5–6 animals/group, 100 cells/animal). C, Traf3ip2 gene deletion attenuates I/R-induced MMP2 and MMP9 activation. After indicated reperfusion periods, non-ischemic zones were analyzed for MMP activation by immunoblotting using antibodies that detect both pro and active forms (n = 3/group). D, Traf3ip2 gene deletion attenuates I/R-induced fibrosis. After a 12-week reperfusion, fibrosis in non-ischemic zones was analyzed by Picrosirius Red staining. Although representative images are shown on the left, mean collagen positive area is summarized on the right (n = 5–6/group). *, p < at least 0.05 versus respective sham-operated group; †, p < 0.05 versus control-I/R.