Gonadotropin-releasing hormone agonist induces apoptosis and reduces cell proliferation in eutopic endometrial cultures from women with endometriosis

Extended estrogen administration for women with thin endometrium in frozen-thawed in-vitro fertilization programs

“…Women who used GnRHa for pituitary desensitization were found to have a decreased endometrial thickness [24,25]. GnRHa was reported to have adverse effects on endometrial development by enhancing the endometrial cell apoptosis, decreasing the release of pro-mitogenic cytokines such as IL-1β and vascular endothelial growth factor (VEGF), and decreasing the endometrial cells proliferation [24][25][26]. Besides, the down regulation by GnRHa was also reported to decrease the uterine and ovarian blood flow by increasing the vascular resistance index via its effect on pelvic vascular smooth muscle cells [27].…”

Effects of hormonal treatment on nerve fibers in endometrium and myometrium in women with endometriosis

“…Combined OCs increased apoptosis and decreased Bcl-2 expression in eutopic endometrium in women with endometriosis (5), and progestogen combined with E 2 decreased the expression of Bcl-2 in the rat endometrium (33). Gonadotropin-releasing hormone analogues also induced apoptosis (34) and decreased Bcl-2 expression in eutopic endometrium in women with endometriosis (35). Combined OCs also significantly reduced glandular VEGF expression in human endometrium (36,37).…”

Endometriosis and Angiogenic Factors

“…That Lefty-2 was noticeably more abundant in patients with endometriosis who did not conceive compared with those who became pregnant, suggested a role in implantation (Tabibzadeh et al, 2000). More, it has been shown that TGF-ß 1also induces contractions of decidual stromal cells (Kimatrai et al, 2003) and inhibits motility of stromal endometrial cells (Nasu et al, 2005).It is important to show how TGF-ß 1stimulated DNA synthesis in epithelial cells at low concentrations, but inhibited DNA synthesis at higher concentrations in women with and without endometriosis (Meresman et al, 2003). Additional evidence showed that TGF-ß 1induces expression of FasL mRNA and protein in endometrial stromal cells (Garci-Velasco et al, 1999), possibly preventing apoptosis during transit to the peritoneal cavity.…”