Cardiac Hypertrophy and Regresion during Postpartum in C57B1/6 Mice
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Cardiac hypertrophy is an increase in heart size due to either physiological or pathological reasons. Physiological inducers include exercise or pregnancy. For instance, athletes experience cardiac hypertrophy during their seasons of workouts. However, when they stop working out consistently, their hearts undergo cardiac regression, the decrease of heart size back to normal. This regression also happens after a woman delivers a baby. However, hypertrophy may still continue throughout breastfeeding; in such cases, regression would occur after lactation has ended. Although cardiac hypertrophy has been extensively researched, hypertrophy during lactation and the regression of hypertrophy has been significantly less investigated. Thus, the objective of this study was to evaluate changes in the heart mass after pregnancy-induced cardiac hypertrophy, and identify the signaling pathways responsible for these changes. Mice were divided into the following groups: control (non-pregnant diestrus cycle), 17 days of gestation (late stage of pregnancy), 7 days of postpartum, 21 days of postpartum (time of weaning), 7 days after weaning, and 21 days after weaning. We hypothesized that the heart size would increase throughout pregnancy and even more so during lactation by modifying pro-hypertrophic signaling pathways, and then it would decrease in size after weaning by altering pro-atrophic signaling. We found that lactation further increases pregnancy-induced cardiac hypertrophy. In addition, signaling pathways including phosphorylated FoxO and ERK were significantly increased during lactation. Cardiac regression begins to occur after the lactation period has ended, but hearts did not regress completely back to normal after 3 weeks of weaning. Our results suggest that lactation further increases pregnancy-induced cardiac hypertrophy and this is mediated by inactivation of FoxO and ERK signaling pathways.