Early post‐myocardial infarction survival in MRL mice is mediated by attenuated apoptosis and inflammation but depends on genetic background

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The Murphy Roth Large (MRL) mouse, a strain capable of regenerating right ventricular myocardium, has a high post‐ myocardial infarction (MI) survival rate compared with C57BL/6J (C57) mice. The biological processes responsible for this advantage are unknown. To assess the effect of genetic background, the LG/J strain, which provides 75% of the MRL composite genome, was included in the study. The MRL survival advantage versus C57 mice ( P = 0.01) occurred largely in the first 5 days; LG/J survival was intermediate ( P = NS). Analysis and annotation of microarray data revealed significantly attenuated acute apoptotis ( P < 0.05) and delayed expression of stress response transcripts in MRL hearts compared to C57 hearts. Supporting the microarray results, there were fewer TUNEL‐positive cells 1 day post‐MI ( P < 0.05) and fewer CD45‐positive inflammatory cells in MRL hearts 2 days post‐MI ( P < 0.01) compared to the C57. Chronically, MRL hearts had smaller infarct scars and attenuated ventricular dilation 30 days post‐MI than C57 hearts ( P < 0.05). We conclude that the early post‐MI survival advantage of MRL mice over the C57 strain is mediated at least in part by reductions in apoptosis and inflammatory infiltration, and that this may influence chronic remodeling. The intermediate survival rate of LG/J mice suggests the high tolerance for MI in the MRL could be derived from its shared genetic background with the LG/J. Support: NIH

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