Gonadotropin-releasing hormone analog repairs reduced endometrial cell apoptosis in endometriosis in vitro

A Imai, Atsushi Imai, Imai A, Atsushi Takagi, Takagi A, A Takagi, T Tamaya, Tamaya T, Teruhiko Tamaya
American Journal of Obstetrics and Gynecology · 2000 · vol. 182(5) , pp. 1142–1146 · doi:10.1067/mob.2000.104804 · PMID:10819849 · W2001135993
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This study investigated how a gonadotropin-releasing hormone analog affects apoptosis in endometrial cells cultured in vitro from women with endometriosis, finding it reverses reduced apoptosis.

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Abstract

ObjectiveImpaired sensitivity of endometrial tissue to spontaneous apoptosis in women with endometriosis contributes to the abnormal implantation and growth of endometrium at ectopic sites. Our purpose was to examine the effect of gonadotropin-releasing hormone analog, widely used in the treatment of endometriosis, on the reduced rate of endometrial apoptosis in endometriosis.Study designPaired ectopic and eutopic endometrial tissue specimens were obtained from 13 patients with endometriosis, and control samples were taken from 8 patients with uterine myoma. Apoptotic cell death was assessed biochemically and morphologically with an enzyme-linked immunoassay and Hoechst No. 33342 staining of deoxyribonucleic acid fragment, respectively.ResultsSpontaneous apoptosis was significantly lower in ectopic and eutopic endometrial tissue from patients with endometriosis (0.22 +/- 0.082 in absorbance) than in endometrial tissue from control subjects (0.52 +/- 0.483)(P < 0.001). Incubation with a gonadotropin-releasing hormone analog (1 micromol/L) increased the apoptotic rate of endometrial cells from patients with endometriosis to 0.56 +/- 0.501 (P <.001). The effect of this gonadotropin-releasing hormone revealed a dose dependency; a half-maximal effect occurred with 10 nmol/L; however, the control endometrium was not affected.ConclusionExposure to gonadotropin-releasing hormone results in changes of the sensitivity of endometriotic endometrium to spontaneous apoptosis; these changes in sensitivity may, in turn, release endometrial cells from resistance to apoptosis and result in reduced survival and growth. This phenomenon could, at least in part, account for the therapeutic action of gonadotropin-releasing hormone analog on endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Apoptosis Buserelin Endometriosis Endometrium Leuprolide Apoptosis Benzimidazoles Buserelin Coloring Agents DNA Fragmentation Endometriosis Endometrium Enzyme-Linked Immunosorbent Assay Female Fluorescent Dyes Humans Leuprolide Propidium

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