Progesterone-dependent regulation of endometrial cannabinoid receptor type 1 (CB1-R) expression is disrupted in women with endometriosis and in isolated stromal cells exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)
The above title was published in Fertility and Sterility in 2012 and can be found on PubMed.
The research finds that endometriosis, where cells grow outside instead of inside the uterus (endometrium), is caused by a failure to communicate between progesterone and the cannabinoid system; this failure is painful and contributes to infertility. Summary quote from the research: “Our studies reveal a role for the anti-inflammatory actions of progesterone in regulating endometrial cannabinoid signaling, which is disrupted in women with endometriosis.”
How does that work though? What is disrupted? If communication between progesterone and the CB1 receptor is disrupted (as cells grow, just in the wrong place), how do cells normally communicate in a healthy, undisrupted homeostatic way?
The answer involves cannabinoid and progesterone nuclear receptor signaling: let’s just begin there next week.
*Next Up: 31 May and a homeostatic view of Progesterone Nuclear Receptors and Cannabinoid Systems.
Posted by Bryan W. Brickner