PMID- 34816741
OWN - NLM
STAT- MEDLINE
DCOM- 20211125
LR  - 20220531
IS  - 1473-2300 (Electronic)
IS  - 0300-0605 (Print)
IS  - 0300-0605 (Linking)
VI  - 49
IP  - 11
DP  - 2021 Nov
TI  - Chemerin regulates autophagy to participate in polycystic ovary syndrome.
PG  - 3000605211058376
LID - 10.1177/03000605211058376 [doi]
LID - 03000605211058376
AB  - 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.
FAU - Luo, Xiaodong
AU  - Luo X
AD  - Department of Obstetrics and Gynecology, 585250The Second Affiliated Hospital of 
      Chongqing Medical University, The Second Affiliated Hospital of Chongqing Medical 
      University, Yuzhong District, Chongqing, P. R. China.
FAU - Gong, Yangyang
AU  - Gong Y
AD  - Department of Obstetrics and Gynecology, 585250The Second Affiliated Hospital of 
      Chongqing Medical University, The Second Affiliated Hospital of Chongqing Medical 
      University, Yuzhong District, Chongqing, P. R. China.
FAU - Cai, Liuyun
AU  - Cai L
AD  - Department of Obstetrics and Gynecology, 585250The Second Affiliated Hospital of 
      Chongqing Medical University, The Second Affiliated Hospital of Chongqing Medical 
      University, Yuzhong District, Chongqing, P. R. China.
FAU - Zhang, Lei
AU  - Zhang L
AD  - Department of Obstetrics and Gynecology, 585250The Second Affiliated Hospital of 
      Chongqing Medical University, The Second Affiliated Hospital of Chongqing Medical 
      University, Yuzhong District, Chongqing, P. R. China.
FAU - Dong, Xiaojing
AU  - Dong X
AUID- ORCID: 0000-0001-8506-9362
AD  - Department of Obstetrics and Gynecology, 585250The Second Affiliated Hospital of 
      Chongqing Medical University, The Second Affiliated Hospital of Chongqing Medical 
      University, Yuzhong District, Chongqing, P. R. China.
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Int Med Res
JT  - The Journal of international medical research
JID - 0346411
RN  - 0 (Chemokines)
RN  - 0 (Cmklr1 protein, rat)
RN  - 0 (Rarres2 protein, rat)
RN  - 0 (Receptors, Chemokine)
SB  - IM
MH  - Animals
MH  - *Autophagy
MH  - *Chemokines/genetics
MH  - Disease Models, Animal
MH  - Female
MH  - Granulosa Cells
MH  - Humans
MH  - Phosphatidylinositol 3-Kinases/genetics
MH  - *Polycystic Ovary Syndrome/genetics
MH  - Rats
MH  - Receptors, Chemokine
PMC - PMC8647268
OTO - NOTNLM
OT  - CMKLR1
OT  - COV434 granulosa cell
OT  - Polycystic ovary syndrome
OT  - autophagy
OT  - chemerin
OT  - mammalian target of rapamycin
COIS- Declaration of conflicting interest: The authors declare that there is no 
      conflict of interest.
EDAT- 2021/11/25 06:00
MHDA- 2021/11/26 06:00
PMCR- 2021/11/24
CRDT- 2021/11/24 08:44
PHST- 2021/11/24 08:44 [entrez]
PHST- 2021/11/25 06:00 [pubmed]
PHST- 2021/11/26 06:00 [medline]
PHST- 2021/11/24 00:00 [pmc-release]
AID - 10.1177_03000605211058376 [pii]
AID - 10.1177/03000605211058376 [doi]
PST - ppublish
SO  - J Int Med Res. 2021 Nov;49(11):3000605211058376. doi: 10.1177/03000605211058376.