Regulation of Alpha‐Myosin Heavy Chain in cardiac remodeling associated with pregnancy

During pregnancy, an increase in blood volume occurs to compensate for fetal development, resulting in adaptive cardiac hypertrophy, which typically remodels back to pre‐pregnancy size shortly after the mother gives birth. In contrast, pathologic cardiac hypertrophy may begin as a compensatory process, but transitions to a maladaptive state and can lead to heart failure. During pathologic cardiac hypertrophy, levels of MHC are altered: beta‐myosin heavy chain (β‐MHC) is increased and alpha‐myosin heavy chain (α‐MHC) is decreased. Activation of α‐MHC in animal models of heart failure has been shown to preserve cardiac function and prevent of heart failure. Interestingly, we have shown that α‐MHC is upregulated in the heart during pregnancy in a rat model, potentially contributing to preserved heart function and adaptive remodeling typically associated with pregnancy. We propose that by studying the mechanisms of α‐MHC regulation that aid in adaptive cardiac remodeling associated with pregnancy, we will gain a better understanding of mechanisms to promote adaptive remodeling in pathologic situations. To characterize the regulation of MHC and MHC regulatory factors that occur during pregnancy induced cardiac remodeling, we subjected rats to timed matings and collected morphological and biochemical data from not pregnant, 19 days pregnant, and 24 hours postpartum. Our rat model for pregnancy induced hypertrophy demonstrated that heart size and weight is increased at 19 days pregnant, and begins to return to normal 24 hours postpartum. Real‐time PCR analysis revealed unique expression patterns of MHC genes and regulatory factors in the hearts of non‐pregnant, late pregnant, and postpartum rats.