Heightened uterine mammalian target of rapamycin complex 1 (mTORC1) signaling provokes preterm birth in mice.

Abstract:

:Although preterm delivery is a major global health issue, its causes and underlying mechanism remain elusive. Using mutant mice, mimicking aspects of human preterm birth, we show here that uterine decidual senescence early in pregnancy via heightened mammalian target of rapamycin complex 1 (mTORC1) signaling is a significant contributor of preterm birth and fetal death, and that these adverse phenotypes are rescued by a low dose of rapamycin, an inhibitor of mTORC1 signaling. This role of mTORC1 signaling in determining the timing of birth in mice may help us better understand the mechanism of the timing of birth in humans and develop new and improved strategies to combat the global problem of preterm birth.

authors

Hirota Y,Cha J,Yoshie M,Daikoku T,Dey SK

doi

10.1073/pnas.1108180108

subject

Has Abstract

pub_date

2011-11-01 00:00:00

pages

18073-8

issue

44

eissn

0027-8424

issn

1091-6490

pii

1108180108

journal_volume

108

pub_type

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