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Autotaxin-lysophosphatidic acid-LPA(3) signaling at the embryo-epithelial
boundary controls decidualization pathways
#MMPMID28588064
Aikawa S
; Kano K
; Inoue A
; Wang J
; Saigusa D
; Nagamatsu T
; Hirota Y
; Fujii T
; Tsuchiya S
; Taketomi Y
; Sugimoto Y
; Murakami M
; Arita M
; Kurano M
; Ikeda H
; Yatomi Y
; Chun J
; Aoki J
EMBO J
2017[Jul]; 36
(14
): 2146-2160
PMID28588064
show ga
During pregnancy, up-regulation of heparin-binding (HB-) EGF and cyclooxygenase-2
(COX-2) in the uterine epithelium contributes to decidualization, a series of
uterine morphological changes required for placental formation and fetal
development. Here, we report a key role for the lipid mediator lysophosphatidic
acid (LPA) in decidualization, acting through its G-protein-coupled receptor
LPA(3) in the uterine epithelium. Knockout of Lpar3 or inhibition of the
LPA-producing enzyme autotaxin (ATX) in pregnant mice leads to HB-EGF and COX-2
down-regulation near embryos and attenuates decidual reactions. Conversely,
selective pharmacological activation of LPA(3) induces decidualization via
up-regulation of HB-EGF and COX-2. ATX and its substrate lysophosphatidylcholine
can be detected in the uterine epithelium and in pre-implantation-stage embryos,
respectively. Our results indicate that ATX-LPA-LPA(3) signaling at the
embryo-epithelial boundary induces decidualization via the canonical HB-EGF and
COX-2 pathways.
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