10.5061/DRYAD.HB0338G
Dai, Qunsheng
Duke University
Likes, Creighton E
Duke University
Luz, Anthony L
Duke University
Mao, Lan
Duke University
Yeh, Jason S
Duke University
Wei, Zhengzheng
Duke University
Kuchibhatla, Maragatha
Duke University
Ilkayeva, Olga R
Duke University
Koves, Timothy R
Duke University
Price, Thomas M
Duke University
Data from: A mitochondrial progesterone receptor increases cardiac
beta-oxidation and remodeling
Dryad
dataset
2019
mouse
heart function
mitochondrial progesterone receptor
beta oxidation
cellular respiration
National Science Foundation
https://ror.org/021nxhr62
na
2019-01-10T01:02:30Z
2019-01-10T01:02:30Z
en
https://doi.org/10.1210/js.2018-00219
3117515 bytes
1
CC0 1.0 Universal (CC0 1.0) Public Domain Dedication
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.
SupplementalSupplemental methods, data and result
na