The effect of estradiol on the production and secretion of complement component 3 by the rat uterus and surgically induced endometriotic tissue

We have recently demonstrated that glandular epithelial cells isolated from human endometriotic tissue synthesize and secrete complement component 3 (C3). Furthermore, because C3 is capable of producing many of the immunological activities known to be associated with human endometriosis, we studied the production, secretion, and regulation of C3 using the rat model for endometriosis. Endometriosis was surgically induced in 20 adult female rats. The animals were then ovariectomized and one half were treated with estradiol (E2) for 3days. Uterine luminal epithelial cells synthesized and secreted C3 only after E2 administration, whereas the uteri from control animals did not produce C3. In contrast, the ectopic endometrium from control animals produced and secreted C3, and this expression was strongly upregulated by in vivo E2 administration. We conclude that surgically induced endometriosis in the rat has properties biochemically independent from the intact uterus and may serve as a useful model to further investigate the regulation of C3 synthesis from human endometriosis.