RBPJ mediates uterine repair in the mouse and is reduced in women with recurrent pregnancy loss.

ABSTRACT: Unexplained recurrent pregnancy loss (uRPL) is associated with repeated embryo loss and endometrial repair with elevated endometrial expression of inflammatory cytokines, including IFN-γ. Notch signaling through its transcription factor recombination signal binding protein Jκ (RBPJ) regulates mechanisms including the immune response and repair after tissue injury. Initially, null mutation of RBPJ in the mouse uterus ( Pgr^cre/+Rbpj^f/f; Rbpj c-KO) results in subfertility, but we have found that these mice become infertile after pregnancy as a result of dysfunctional postpartum uterine repair, including delayed endometrial epithelial and myometrial regeneration. RNA sequencing of postpartum uterine repair sites revealed global up-regulation of inflammatory pathways, incl

SUBMITTER: Strug MR 

PROVIDER: S-EPMC6207278 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature