A Mitochondrial Progesterone Receptor Increases Cardiac Beta-Oxidation and Remodeling.
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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 nonnuclear 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, 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.
Published Version (Please cite this version)10.1210/js.2018-00219
Publication InfoPrice, Thomas; Dai, Qunsheng; Likes, Creighton E; Luz, Anthony L; Mao, Lan; Yeh, Jason S; ... Koves, Timothy R (2019). A Mitochondrial Progesterone Receptor Increases Cardiac Beta-Oxidation and Remodeling. Journal of the Endocrine Society, 3(2). pp. 446-467. 10.1210/js.2018-00219. Retrieved from https://hdl.handle.net/10161/18107.
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Professor of Obstetrics and Gynecology
Dr. Price is involved in both clinical and basic science research. The main focus of the basic science molecular endocrinology laboratory is the study of novel sex steroid receptors. Currently, the work focuses on a novel progesterone receptor that localizes to the mitochondrion. Studies including RNAi in cell models and creation of transgenic mice are ongoing to discover the function of this receptor. The overall hypothesis is that progesterone modulates mitochondrial activity to meet the incre