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Data from: A mitochondrial progesterone receptor increases cardiac beta-oxidation and remodeling

Citation

Dai, Qunsheng et al. (2019), Data from: A mitochondrial progesterone receptor increases cardiac beta-oxidation and remodeling, Dryad, Dataset, https://doi.org/10.5061/dryad.hb0338g

Abstract

Progesterone is primarily a pregnancy related hormone, produced in substantial quantities after ovulation and during gestation. Traditionally known to function via nuclear receptors for transcriptional regulation there is also evidence of non-nuclear action. A previously identified mitochondrial progesterone receptor (PR-M) increases cellular respiration in cell models. In these studies, we demonstrated that expression of PR-M in rat H9c2 cardiomyocytes resulted in a ligand-dependent increase in oxidative cellular respiration and beta-oxidation. Cardiac expression in a TET-On transgenic mouse resulted in gene expression of myofibril proteins for remodeling and proteins involved in oxidative phosphorylation and fatty acid metabolism. In a model of increased afterload from constant transverse aortic constriction (cTAC), mice expressing PR-M showed a ligand-dependent preservation of cardiac function. From these observations, we propose that PR-M is responsible for progesterone-induced increases in cellular energy production and cardiac remodeling to meet the physiological demands of pregnancy.

Usage Notes

Funding

National Science Foundation, Award: na

Location

na