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Publication : Parent-of-origin effects on cardiac response to pressure overload in mice.

First Author  Barrick CJ Year  2009
Journal  Am J Physiol Heart Circ Physiol Volume  297
Issue  3 Pages  H1003-9
PubMed ID  19561308 Mgi Jnum  J:154239
Mgi Id  MGI:4367520 Doi  10.1152/ajpheart.00896.2008
Citation  Barrick CJ, et al. (2009) Parent-of-origin effects on cardiac response to pressure overload in mice. Am J Physiol Heart Circ Physiol 297(3):H1003-9
abstractText  Left ventricular (LV) hypertrophy (LVH) is an independent risk factor for cardiovascular mortality and is commonly caused by hypertension. In rodents, transverse aortic constriction (TAC) is a model regularly employed in mechanistic studies of the response of the LV to pressure overload. We previously reported that inbred strains of male mice manifest different cardiac responses to TAC, with C57BL/6J (B6) developing LV dilatation and impaired contractility and 129S1/SvImJ (129) males displaying concentric LVH. In the present study, we investigated sex and parent-of-origin effects on the response to TAC by comparing cardiac function, organ weights, expression of cardiac hypertrophy markers, and histology in female B6 and female 129 mice and in F1 progeny of reciprocal crosses between B6 and 129 mice (B6129F1 and 129B6F1). Five weeks after TAC, heart weight increased to the greatest extent in 129B6F1 mice and the least extent in 129 and B6129F1 mice. Female 129B6F1 and B6 mice were relatively protected from the increase in heart weight that occurs in their male counterparts with pressure overload. The response to TAC in 129 consomic mice bearing the B6 Y chromosome resembled that of 129 rather than 129B6F1 mice, indicating that the B6 Y chromosome does not account for the differences in the reciprocal cross. Our results suggest that susceptibility to LVH is more complex than simple Mendelian inheritance and that parental origin effects strongly impact the LV response to TAC in these commonly used inbred strains.
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