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Significance Preterm birth is a leading cause of neonatal mortality, with a poorly understood etiology. The maintenance of uterine quiescence across gestation is fundamental for term parturition. At the molecular level, an integrated uterine endoplasmic reticulum stress-unfolded protein response (UPR-ERSR) regulates both caspase-3 (CASP3) and caspase-7 (CASP7), preserving myometrial quiescence throughout gestation. Here we show that prolonged ERSR diminishes the tocolytic potential of uterine CASP3 and 7, causing an increase in myometrial contractile responsiveness and onset of preterm labor in pregnant mice. Prophylaxis with 4-phenylbutrate, however, maintains active uterine CASP3 and 7 and prolongs gestational length. This study establishes a critical role for UPR-ERSR in the regulation of pregnant uterine myocyte quiescence.

Uterine endoplasmic reticulum stress-unfolded protein response regulation of gestational length is caspase-3 and -7–dependent