Autotaxin–Lysophosphatidic Acid–LPA3 Signaling at the Embryo-Epithelial Boundary Controls Decidualization Pathways
June 2017
in “
The EMBO Journal
”
autotaxin lysophosphatidic acid LPA3 decidualization placental formation fetal development Lpar3 knockout HB-EGF COX-2 LPA3 agonist T13 uterine hypertrophy stromal proliferation angiogenesis luminal epithelium breakdown Bmp2 Wnt4 ATX LPA LPA3 receptor placenta formation fetus development LPA3 receptor knockout heparin-binding EGF-like growth factor cyclooxygenase-2 LPA3 receptor activator T13 compound uterus enlargement stromal cell growth blood vessel formation epithelial layer breakdown bone morphogenetic protein 2 wingless-related integration site 4
TLDR LPA3 signaling in the uterus is crucial for placental formation and fetal development.
The study demonstrated that autotaxin-lysophosphatidic acid (LPA) signaling through the LPA3 receptor was crucial for controlling decidualization pathways at the embryo-epithelial boundary, essential for successful implantation and pregnancy. Knockout of Lpar3 or inhibition of autotaxin in pregnant mice led to reduced expression of HB-EGF and COX-2, resulting in impaired decidualization. Activation of LPA3 up-regulated these factors, promoting cell proliferation, angiogenesis, and tissue remodeling. The findings suggested that LPA3 signaling could be a potential target for treating reproductive disorders such as infertility and endometriosis, highlighting its broader role in female reproductive health.
