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 (ESC) decidualization, the role of autophagy in decidualization has remained elusive. To determine the role of autophagy in decidualization, we utilized 2 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, ESCs failed to properly decidualize and fewer blastocysts were able to implant. Additionally, small interfering RNA knock down of Atg16L1 was detrimental to the decidualization response of human ESCs. We conclude that Atg16L1 is necessary for decidualization, implantation, and overall fertility in mice. Furthermore, considering its requirement for human endometrial decidualization, these data suggest Atg16L1 may be a potential mediato...Continue Reading
Alteration of reproductive function but not prenatal sexual development after insertional disruption of the mouse estrogen receptor gene
Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method
Endocannabinoid signaling in synchronizing embryo development and uterine receptivity for implantation
Estrogen is a critical determinant that specifies the duration of the window of uterine receptivity for implantation
Facilitative glucose transporter type 1 is differentially regulated by progesterone and estrogen in murine and human endometrial stromal cells
Female obesity adversely affects assisted reproductive technology (ART) pregnancy and live birth rates
The second European evidence-based Consensus on the diagnosis and management of Crohn's disease: Special situations
Dehydroepiandrosterone inhibits glucose flux through the pentose phosphate pathway in human and mouse endometrial stromal cells, preventing decidualization and implantation
The regulation of embryo implantation and endometrial decidualization by progesterone receptor signaling
Mechanism and functions of membrane binding by the Atg5-Atg12/Atg16 complex during autophagosome formation
Glucosamine inhibits decidualization of human endometrial stromal cells and decreases litter sizes in mice
Acceleration of the glycolytic flux by steroid receptor coactivator-2 is essential for endometrial decidualization
Diet-induced obesity impairs endometrial stromal cell decidualization: a potential role for impaired autophagy
Growth regulation by estrogen in breast cancer 1 (GREB1) is a novel progesterone-responsive gene required for human endometrial stromal decidualization
FOXO1 regulates uterine epithelial integrity and progesterone receptor expression critical for embryo implantation
Distinct functions of ATG16L1 isoforms in membrane binding and LC3B lipidation in autophagy-related processes
Decreased Autophagy Impairs Decidualization of Human Endometrial Stromal Cells: A Role for ATG Proteins in Endometrial Physiology
An autophagic deficit in the uterine vessel microenvironment provokes hyperpermeability through deregulated VEGFA, NOS1, and CTNNB1.
The SARS-CoV-2 receptor, angiotensin-converting enzyme 2, is required for human endometrial stromal cell decidualization†.
AMPK/mTOR downregulated autophagy enhances aberrant endometrial decidualization in folate-deficient pregnant mice.
The discovery of autophagy-related ('ATG') proteins in the 1990s greatly advanced the mechanistic understanding of autophagy and clarified the fact that autophagy serves important roles in various biological processes.
Autophagy & Model Organisms
Autophagy is a cellular process that allows degradation by the lysosome of cytoplasmic components such as proteins or organelles. Here is the latest research on autophagy & model organisms