Developmental Biology
Sustained Endocannabinoid Signaling Compromises Decidual Function and Promotes Inflammation-induced Preterm Birth
Recent studies provide evidence that premature maternal decidual senescence resulting from heightened mTORC1 signaling is a cause of preterm birth (PTB). We show here that mice devoid of fatty acid amide hydrolase (FAAH) with elevated levels of N-arachidonyl ethanolamide (anandamide), a major endocannabinoid lipid mediator, were more susceptible to PTB upon lipopolysaccharide (LPS) challenge. Anandamide is degraded by FAAH and primarily works by activating two G-protein-coupled receptors CB1 and CB2, encoded by Cnr1 and Cnr2, respectively.Muscle Segment Homeobox Genes Direct Embryonic Diapause by Limiting Inflammation in the Uterus
Background: Embryonic diapause is a reproductive strategy that confers blastocyst dormancy and uterine quiescence without implantation until conditions become favorable.Results: Mice devoid of uterine muscle segment homeobox genes (Msx) show heightened inflammatory signature with failure of diapause.Conclusion: Msx coordinates various pathways limiting inflammation in the uterus for diapause.Significance: This study identifies a previously unrecognized role of Msx in this unique phenomenon.
