Differential induction of autophagy by mTOR is associated with abnormal apoptosis in ovarian endometriotic cysts

Jung‐Joo Choi, JongYeob Choi, MinWha Jo, Mun Seok Jo, EunYoung Lee, Eun‐Ju Lee, Hyun Jin Kim, Hyo Jeong Kim, DooSeok Choi
Molecular human reproduction · 2013 · vol. 20(4) , pp. 309–317 · doi:10.1093/molehr/gat091 · PMID:24319109 · W2135948028
article OA: bronze CC0 ⤵ 58 in-corpus citations
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Aberrant mTOR activity in ovarian endometriotic cysts alters endometrial cell autophagy and is associated with abnormal apoptosis, with mTOR inhibition promoting apoptosis via autophagy induction.

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Abstract

Mammalian target of rapamycin (mTOR) is known to be a major negative regulator of autophagy. Recent studies have shown that mTOR activity is abnormally increased in endometriotic lesions. In endometriosis, abnormal mTOR activity may contribute to the alteration of endometrial cell autophagy, which may affect apoptosis because endometrial cell autophagy is directly involved in the regulation of apoptosis. To test this hypothesis, we investigated whether endometrial cell autophagy is altered by aberrant mTOR activity and is associated with apoptosis in ovarian endometriotic cysts. Our results show that endometrial cell autophagy induction was increased by mTOR inhibition as the menstrual cycle progresses in the normal endometrium, and that it is correlated with apoptosis. However, in endometriotic tissues from ovarian endometriotic cysts, autophagy, mTOR activity and apoptosis were constant throughout the menstrual cycle, suggesting that a constant level of autophagy is maintained by disinhibition of mTOR activity during the menstrual cycle in endometriotic tissues and is related to decreased apoptosis. Indeed, compared with normal endometrium, increased mTOR activity during the secretory phase in endometriotic tissues inhibited autophagy and apoptosis induction. In addition, to determine the direct effect of autophagy induction mediated by mTOR on endometriotic cell apoptosis, endometriotic cells were treated with rapamacin (mTOR inhibitor) with and without 3-methyladenine (3-MA, autophagy inhibitor). Although rapamycin treatment induced autophagy and led to apoptosis promotion, the pro-apoptotic effect of rapamycin was reversed by the addition of 3-MA, suggesting that mTOR inhibition promotes endometriotic cell apoptosis via autophagy induction. In conclusion, our results suggest that aberrant mTOR activity in ovarian endometriotic cysts leads to alteration of endometrial cell autophagy, which is associated with abnormal apoptosis.

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Condition tags

endometriosis

MeSH descriptors

Apoptosis Autophagy Cysts Endometriosis TOR Serine-Threonine Kinases Adenine Adenine Adenine Animals Apoptosis Autophagy Cysts Cysts Cysts Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium

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