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. Author manuscript; available in PMC: 2009 May 2.
Published in final edited form as: Cell. 2008 May 2;133(3):462–474. doi: 10.1016/j.cell.2008.02.048

Figure 7. Mice lacking MsrA have increased CaMKII oxidation, apoptosis, reduced survival and impaired heart function after myocardial infarction.

Figure 7

(A) Immunostaining and (B) stain intensity quantification of oxidized CaMKII in heart sections from WT, p47−/−, and MsrA−/− mice post-MI (n = 3 hearts/group, * p < 0.05 vs. WT). (C) Summary data for TUNEL staining of heart sections from WT, p47−/−, and MsrA−/− mice post-MI (n = 3 hearts/group, * p < 0.05 vs. WT). (D) Mortality is significantly increased post-MI in MsrA−/− mice compared to WT controls. Numbers in bars represent post-MI deaths/total number of mice receiving MI. Post-MI left ventricular dilation (E) and function (F) were compromised in surviving MsrA−/− mice compared to WT controls three weeks after surgery (n = 17 hearts/group for WT, n = 9 hearts/group for MsrA−/−).