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Publication : Mice Missing Cnr1 and Cnr2 Show Implantation Defects.

First Author  Li Y Year  2019
Journal  Endocrinology Volume  160
Issue  4 Pages  938-946
PubMed ID  30776303 Mgi Jnum  J:273081
Mgi Id  MGI:6285273 Doi  10.1210/en.2019-00024
Citation  Li Y, et al. (2019) Mice Missing Cnr1 and Cnr2 Show Implantation Defects. Endocrinology 160(4):938-946
abstractText  Cannabinoid/endocannabinoid signaling is primarily mediated by cannabinoid receptor type 1 (CB1; encoded by Cnr1) and/or type 2 (CB2; encoded by Cnr2). Here, we show that Cnr1-/-Cnr2-/- mice are subfertile as a result of compromised implantation. Upon implantation, the epithelium is smooth and adhered to the blastocyst trophectoderm within the implantation chamber (crypt) in wild-type mice, whereas the epithelium in Cnr1-/-Cnr2-/- mice is ruffled, which compromises appropriate blastocyst-uterine interactions. The suboptimal implantation leads to higher incidence of pregnancy failure in Cnr1-/-Cnr2-/- mice. Histological analysis revealed heightened edema around the implantation chamber in these deleted females. With the use of a reporter mouse line, we observed that CB2 is present on endothelial cells of uterine blood vessels, and its absence leads to blood vessel leakage during implantation. These results suggest that appropriately regulated uterine edema is important to optimal implantation.
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