Varying susceptibility to myocardial infarction among C57BL/6 mice of different genetic background.

Abstract	Genetically manipulated mouse lines are invaluable to investigate the effects of a single gene on sensitivity to ischemia. When choosing appropriate controls, we were concerned that intrinsic, strain-independent but colony-dependent differences may influence the susceptibility to ischemia. We, therefore, compared the infarct:risk volume ratio (I:R%) after 30-min global ischemia in Langendorff-perfused hearts from outbred C57BL/6 mice with that in wild-type mice derived from heterozygote x heterozygote crosses of two different in-house C57BL/6 mouse lines with targeted disruption of an MKK3 or MAPKAPK2 allele. Despite similar hemodynamic characteristics, I:R% in outbred C57BL/6 hearts was significantlysmaller (40.8 +/- 2.8%) than in C57BL/6 MAPKAPK2 wild types (65.8 +/- 4.5%, P = 0.0003) and significantly larger than in C57BL/6 MKK3 wild types (23.7 +/- 2.9%, P = 0.002). Therefore, inherent colony substrain-dependent differences appear to influence the susceptibility to infarction in response to global ischemia, underscoring the importance of using colony-matched wild-type controls in murine studies of myocardial ischemia.
Authors	Diana A Gorog, Masaya Tanno, Alamgir M N Kabir, Gajen S Kanaganayagam, Rekha Bassi, Simon G Fisher, Michael S Marber
Journal	Journal of molecular and cellular cardiology (J Mol Cell Cardiol) Vol. 35 Issue 6 Pg. 705-8 (Jun 2003) ISSN: 0022-2828 [Print] England
PMID	12788388 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Intracellular Signaling Peptides and Proteins MAP-kinase-activated kinase 2 Protein-Tyrosine Kinases Protein Serine-Threonine Kinases MAP Kinase Kinase 3 Map2k3 protein, mouse Mitogen-Activated Protein Kinase Kinases
Topics	Alleles Animals Female Genetic Predisposition to Disease Heterozygote Homozygote Intracellular Signaling Peptides and Proteins MAP Kinase Kinase 3 Male Mice Mice, Inbred C57BL Mice, Knockout Mitogen-Activated Protein Kinase Kinases (genetics) Myocardial Infarction (genetics) Perfusion Protein Serine-Threonine Kinases (genetics) Protein-Tyrosine Kinases (genetics) Species Specificity

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