Hoxa-10 deficiency alters region-specific gene expression and perturbs differentiation of natural killer cells during decidualization.

ABSTRACT: Uterine decidualization, a key event for successful implantation, is critically controlled by stromal cell proliferation and differentiation. One hallmark event of decidualization is the acquisition of stromal cell polyploidy through terminal differentiation at the anti-mesometrial pole of the implantation site. Hoxa-10, a developmentally regulated homeobox transcription factor, is highly expressed in decidualizing stromal cells, and targeted deletion of Hoxa-10 in mice shows severe decidualization defects, primarily due to reduced stromal cell responsiveness to progesterone. However, the underlying molecular mechanism by which Hoxa-10 regulates this process remains largely unknown. Here, we show that Hoxa-10 deficiency confers diminished core cell cycle activity during stromal cell prolif

SUBMITTER: Rahman MA 

PROVIDER: S-EPMC4265803 | biostudies-literature | 2006 Feb

REPOSITORIES: biostudies-literature