[Investigation of the apoptosis and proliferation in endometriotic cells].

OBJECTIVE: To clarify whether apoptosis is involved in endometriosis and the effects of estradiol, progesterone and mifepristone on the expression of epidermal growth factor receptor(EGFR) in cultured human endometriotic cells. METHODS: Apoptosis index and bcl-2 gene expression were examined in cultured ectopic endometrial cells from women with endometriosis (n = 15 samples) and compared with eutopic endometrial cells from non-endometriosis cases(n = 11 samples). Apoptotic cells were detected by flowcytometry; bcl-2 gene expression demonstrated by in situ hybridization technique. The cultured endometriotic cells were stimulated by estradiol(E2, 10 nmol/L), progesterone(P, 100 nmol/L), and P + mifepristone(P 100 nmol/L + mifepristone 1,000 nmol/L) respectively for 5 days, the expression of EGFR mRNA of endometriotic cells were determined by reverse transcript polymerase chain reaction (RT-PCR) method. RESULTS: The apoptosis index was significantly decreased in the ectopic endometrial cells [(2.74 +/- 1.54)%] as compared to eutopic endometrial cells [(9.97 +/- 1.26)%] (P < 0.05). bcl-2 expression in endometriotic cells was significantly increased compared with the eutopic endometrial cells (P < 0.05). The expression of EGFR mRNA in E2, P group was 1.10 +/- 0.19 and 1.28 +/- 0.24 respectively, which were significantly higher than that of control(0.90 +/- 0.10, P < 0.01). In P + mifepristone group it was 0.63 +/- 0.11, significantly lower than that of control(P < 0.001). CONCLUSION: The resistance of endometriotic cells to apoptosis may be fundamental in the aetiology and (or) pathophysiology of endometriosis. Estradiol and progesterone promote hyperplasia and differentiation of endometriotic cells while mifepristone inhibits.