A Mitochondrial Progesterone Receptor Increases Cardiac Beta-Oxidation and Remodeling.
J Endocr Soc
; 3(2): 446-467, 2019 Feb 01.
Article
em En
| MEDLINE
| ID: mdl-30746505
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 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.
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1
Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Revista:
J Endocr Soc
Ano de publicação:
2019
Tipo de documento:
Article