Nrf2 regulates gene-environment interactions in an animal model of intrauterine inflammation: Implications for preterm birth and prematurity.

ABSTRACT: Preterm birth (PTB) is the leading cause of neonatal mortality, and surviving infants are at increased risk for lifelong disabilities. Intrauterine inflammation is an etiological factor that drives PTB, and oxidative stress is associated with PTB. Nuclear erythroid 2-related factor 2 (Nrf2) is a redox-sensitive transcription factor that is the key regulator of the response to oxidative and inflammatory stress. Here, we used the established mouse model of intrauterine inflammation-induced PTB to determine whether Nrf2 is a modifier of susceptibility to PTB and prematurity-related morbidity and mortality in the offspring. We determined that Nr2-deficient (Nrf2^-/-) mice exhibited a greater sensitivity to intrauterine inflammation, as indicated by decreased time to delivery, reduced

SUBMITTER: Sussan TE 

PROVIDER: S-EPMC5223218 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature