Chemerin regulates autophagy to participate in polycystic ovary syndrome

Objective Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder in women of reproductive age. Chemerin has recently been discovered as a novel adipokine associated with obesity and metabolic syndrome. Excessive autophagy activity and overexpression of autophagy-related genes in follicul...

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Autores principales:	Xiaodong Luo, Yangyang Gong, Liuyun Cai, Lei Zhang, Xiaojing Dong
Formato:	article
Lenguaje:	EN
Publicado:	SAGE Publishing 2021
Materias:	Medicine (General) R5-920
Acceso en línea:	https://doaj.org/article/cf8baf569bd64acbaba68018edffc421
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spelling	oai:doaj.org-article:cf8baf569bd64acbaba68018edffc4212021-12-02T03:04:38ZChemerin regulates autophagy to participate in polycystic ovary syndrome1473-230010.1177/03000605211058376https://doaj.org/article/cf8baf569bd64acbaba68018edffc4212021-11-01T00:00:00Zhttps://doi.org/10.1177/03000605211058376https://doaj.org/toc/1473-2300Objective Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder in women of reproductive age. Chemerin has recently been discovered as a novel adipokine associated with obesity and metabolic syndrome. Excessive autophagy activity and overexpression of autophagy-related genes in follicular granulosa cells are important mechanisms of PCOS. This study aimed to investigate the effect of chemerin on autophagy in PCOS. Methods A rat model of PCOS was established by subcutaneous injection of testosterone propionate under a high-fat diet. Expression levels of chemerin and its receptor CMKLR1 were determined by real-time polymerase chain reaction and western blot. Proliferation and apoptosis of human granulosa cells in vitro and expression of autophagy-related genes were examined using bafilomycin A1 (autophagy inhibitor) and Torin1 (autophagy inducer). Results Chemerin and CMKLR1 expression were significantly increased in the ovary in a rat model of PCOS. Ectopic expression of chemerin promoted the proliferation and inhibited the apoptosis of COV434 cells. Ectopic expression of chemerin also induced autophagy by inhibiting the phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway. Conclusions Chemerin and CMKLR1 were overexpressed in PCOS rats. Chemerin promoted autophagy through inhibiting the PI3K/Akt/mTOR pathway, and may provide a potential target and biomarker of PCOS.Xiaodong LuoYangyang GongLiuyun CaiLei ZhangXiaojing DongSAGE PublishingarticleMedicine (General)R5-920ENJournal of International Medical Research, Vol 49 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine (General) R5-920
spellingShingle	Medicine (General) R5-920 Xiaodong Luo Yangyang Gong Liuyun Cai Lei Zhang Xiaojing Dong Chemerin regulates autophagy to participate in polycystic ovary syndrome
description	Objective Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder in women of reproductive age. Chemerin has recently been discovered as a novel adipokine associated with obesity and metabolic syndrome. Excessive autophagy activity and overexpression of autophagy-related genes in follicular granulosa cells are important mechanisms of PCOS. This study aimed to investigate the effect of chemerin on autophagy in PCOS. Methods A rat model of PCOS was established by subcutaneous injection of testosterone propionate under a high-fat diet. Expression levels of chemerin and its receptor CMKLR1 were determined by real-time polymerase chain reaction and western blot. Proliferation and apoptosis of human granulosa cells in vitro and expression of autophagy-related genes were examined using bafilomycin A1 (autophagy inhibitor) and Torin1 (autophagy inducer). Results Chemerin and CMKLR1 expression were significantly increased in the ovary in a rat model of PCOS. Ectopic expression of chemerin promoted the proliferation and inhibited the apoptosis of COV434 cells. Ectopic expression of chemerin also induced autophagy by inhibiting the phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway. Conclusions Chemerin and CMKLR1 were overexpressed in PCOS rats. Chemerin promoted autophagy through inhibiting the PI3K/Akt/mTOR pathway, and may provide a potential target and biomarker of PCOS.
format	article
author	Xiaodong Luo Yangyang Gong Liuyun Cai Lei Zhang Xiaojing Dong
author_facet	Xiaodong Luo Yangyang Gong Liuyun Cai Lei Zhang Xiaojing Dong
author_sort	Xiaodong Luo
title	Chemerin regulates autophagy to participate in polycystic ovary syndrome
title_short	Chemerin regulates autophagy to participate in polycystic ovary syndrome
title_full	Chemerin regulates autophagy to participate in polycystic ovary syndrome
title_fullStr	Chemerin regulates autophagy to participate in polycystic ovary syndrome
title_full_unstemmed	Chemerin regulates autophagy to participate in polycystic ovary syndrome
title_sort	chemerin regulates autophagy to participate in polycystic ovary syndrome
publisher	SAGE Publishing
publishDate	2021
url	https://doaj.org/article/cf8baf569bd64acbaba68018edffc421
work_keys_str_mv	AT xiaodongluo chemerinregulatesautophagytoparticipateinpolycysticovarysyndrome AT yangyanggong chemerinregulatesautophagytoparticipateinpolycysticovarysyndrome AT liuyuncai chemerinregulatesautophagytoparticipateinpolycysticovarysyndrome AT leizhang chemerinregulatesautophagytoparticipateinpolycysticovarysyndrome AT xiaojingdong chemerinregulatesautophagytoparticipateinpolycysticovarysyndrome
_version_	1718402009620545536

Chemerin regulates autophagy to participate in polycystic ovary syndrome

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