Pregnancy‐induced physiological cardiac hypertrophy regulates the expression of perilipin isoforms

Abstract

Perilipins (PLINs) isoforms are proteins associated to surface of intracelular lipid droplets (LDs) that participate in the regulation of lipid metabolism and storage during hypertrophic cardiomyopathies. PLINs can associate to the PPAR coactivators peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PGC‐1α) and Sirtuin 1 (SIRT1) to regulate the expression of genes involved in lipid metabolism. Pregnancy‐induced physiological cardiac hypertrophy is a reversible process in which there is a change in lipid metabolism. However, there are a lack attention of the participation of PLINs isoforms in response to pregnancy‐induced cardiac hypertrophy. In this work, we quantified the PLINs isoforms and PGC‐1α mRNAs and proteins level, along with the transcriptional activities de PPARs family, triacylglyceride (TAG) and cholesterol/ester cholesterol in left ventricle of rats before, during, and after pregnancy. Expressions of mRNAs for PLIN1, PLIN2 and PLIN5 increased 9.5‐ and 7.4‐fold, 27.5‐ and 17.7‐fold, and 8‐ and 2.4‐fold 2 during pregnancy and postpartum, respectively, while PLIN3 did not change and PLIN4 was not detected. In contrast, the protein content of PLIN2 increased 1.5‐fold during postpartum, and PLIN5 increased 1.3‐ and 1.5‐ fold during pregnancy and postpartum, respectively, while PLIN1 did not change. Expression of mRNA and protein content for PGC‐1α increased 17.7 and 11.26‐fold and 1.5‐ and 1.2‐ fold during pregnancy and postpartum, respectively. The activity of PPARγ increased 1.6‐fold during pregnancy and decreased to basal levels postpartum. The concentration of TAG and Cholesterol/Cholesteryl ester increased 1.5‐ and 1.4‐ fold in the pregnant group compared to the non‐pregnant group, and returned to basal levels at postpartum, respectively. The results demonstrate that pregnancy‐induced, physiological cardiac hypertrophy activates the expression of genes involved in lipid storage suggesting that the shift in cardiac metabolism is mediated by the activation of PPARγ/PGC‐1α.