Excessive oxidative stress in cumulus granulosa cells induced cell senescence contributes to endometriosis-associated infertility

Xiang Lin, Yongdong Dai, Xiaomei Tong, Wenzhi Xu, Qianmeng Huang, Xiaoying Jin, Chao Li, Feng Zhou, Hanjin Zhou, Xiaona Lin, Dong Huang, Songying Zhang
Redox biology · 2020 · vol. 30 , pp. 101431 · doi:10.1016/j.redox.2020.101431 · PMID:31972508 · PMC6974790 · W2999372282
article OA: gold CC0 ⤵ 60 in-corpus citations
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This study found that excessive oxidative stress induces senescence in cumulus granulosa cells via endoplasmic reticulum stress, contributing to endometriosis-associated infertility.

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Abstract

Endometriosis an important cause of female infertility and seriously impact physical and psychological health of patients. Endometriosis is now considered to be a public health problem that deserves in-depth investigation, especially the etiopathogenesis of endometriosis-associated infertility. We aimed to illuminate the etiopathogenesis of endometriosis-associated infertility that involve excessive oxidative stress (OS) induced pathological changes of ovary cumulus granulosa cell (GCs). Senescence-associated β-galactosidase (SA β-gal) activity in GCs from endometriosis patients, soluble isoform of advanced glycation end products receptor (sRAGE) expression in follicular fluid from endometriosis patients and differentially expressed senescence-associated secretory phenotype factors (IL-1β, MMP-9, KGF and FGF basic protein) are all useful indexes to evaluate oocyte retrieval number and mature oocyte number. RNA-sequencing and bioinformatics analysis indicated senescent phenotype of endometriosis GCs and aggravated endoplasmic reticulum (ER) stress in endometriosis GCs. Targeting ER stress significantly alleviated OS-induced GCs senescence as well as mitochondrial membrane potential (MMP) and adenosine triphosphate (ATP) reduction in GCs. Moreover, melatonin administration rescued OS-enhanced ER stress, cellular senescence, and MMP and ATP abnormities of endometriosis GCs in vitro and in vivo. In conclusion, our results indicated excessive reactive oxygen species induces senescence of endometriosis GCs via arouse ER stress, which finally contributes to endometriosis-associated infertility, and melatonin may represent a novel adjuvant therapy strategy for endometriosis-associated infertility.

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Condition tags

endometriosisinfertility

MeSH descriptors

Antigens, Neoplasm Cumulus Cells Endometriosis Infertility, Female Melatonin Mitogen-Activated Protein Kinases Oxidative Stress Animals Antigens, Neoplasm Cell Line Cellular Senescence Cellular Senescence Cumulus Cells Cumulus Cells Disease Models, Animal Endometriosis Endometriosis Endometriosis Female Gene Expression Profiling

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