The autophagy gene Atg16L1 is necessary for endometrial decidualization.

The autophagy gene Atg16L1 is necessary for endometrial decidualization. Endocrinology. 2019 Dec 26;: Authors: Oestreich AK, Chadchan SB, Popli P, Medvedeva A, Rowen MN, Stephens CS, Xu R, Lydon JP, Demayo FJ, Jungheim ES, Moley KH, Kommagani R Abstract Uterine receptivity is critical for establishing and maintaining pregnancy. For the endometrium to become receptive, stromal cells must differentiate into decidual cells capable of secreting factors necessary for embryo survival and placental development. Although there are multiple reports of autophagy induction correlated with endometrial stromal cell decidualization, the role of autophagy in decidualization remained elusive. To determine the role of autophagy in decidualization, we utilized two genetic models carrying mutations to the autophagy gene Atg16L1. Although the hypomorphic Atg16L1 mouse was fertile and displayed proper decidualization, conditional knockout in the reproductive tract of female mice reduced fertility by decreasing the implantation rate. In the absence of Atg16L1, endometrial stromal cells failed to properly decidualize and fewer blastocysts were able to implant. Additionally, siRNA knock down of Atg16L1 was detrimental to the decidualization response of human endometrial stromal cells. We conclude that Atg16L1 is necessary for decidualization, implantation, and overall fertility in mice. Furthermore, considering its requirement for human endometrial decidual...
Source: Endocrinology - Category: Endocrinology Authors: Tags: Endocrinology Source Type: research