A Mitochondrial Progesterone Receptor Increases Cardiac Beta-Oxidation and Remodeling.


Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Dai, Q; Likes, CE; Luz, AL; Mao, L; Yeh, JS; Wei, Z; Kuchibhatla, M; Ilkayeva, OR; Koves, TR; Price, TM

Published Date

  • February 2019

Published In

Volume / Issue

  • 3 / 2

Start / End Page

  • 446 - 467

PubMed ID

  • 30746505

Pubmed Central ID

  • 30746505

Electronic International Standard Serial Number (EISSN)

  • 2472-1972

International Standard Serial Number (ISSN)

  • 2472-1972

Digital Object Identifier (DOI)

  • 10.1210/js.2018-00219


  • eng