PMID- 35534864
OWN - NLM
STAT- MEDLINE
DCOM- 20220511
LR  - 20220801
IS  - 1478-811X (Electronic)
IS  - 1478-811X (Linking)
VI  - 20
IP  - 1
DP  - 2022 May 9
TI  - Follicular fluid-derived exosomal miR-143-3p/miR-155-5p regulate follicular 
      dysplasia by modulating glycolysis in granulosa cells in polycystic ovary 
      syndrome.
PG  - 61
LID - 10.1186/s12964-022-00876-6 [doi]
LID - 61
AB  - OBJECTIVE: Polycystic ovary syndrome (PCOS) is characterized by follicular 
      dysplasia. An insufficient glycolysis-derived energy supply of granulosa cells 
      (GCs) is an important cause of follicular dysplasia in PCOS. Follicular fluid 
      (FF) exosomal microRNAs (miRNAs) have been proven to regulate the function of 
      GCs. In this study, exosomes extracted from clinical FF samples were used for 
      transcriptome sequencing (RNA-seq) analysis, and a human ovarian granulocyte 
      tumour cell line (KGN cells) was used for in vitro mechanistic studies. METHODS 
      AND RESULTS: In FF exosomal RNA-seq analysis, a decrease in glycolysis-related 
      pathways was identified as an important feature of the PCOS group, and the 
      differentially expressed miR-143-3p and miR-155-5p may be regulatory factors of 
      glycolysis. By determining the effects of miR-143-3p and miR-155-5p on hexokinase 
      (HK) 2, pyruvate kinase muscle isozyme M2 (PKM2), lactate dehydrogenase A (LDHA), 
      pyruvate, lactate and apoptosis in KGN cells, we found that upregulated 
      miR-143-3p expression in exosomes from the PCOS group inhibited glycolysis in KGN 
      cells; knockdown of miR-143-3p significantly alleviated the decrease in 
      glycolysis in KGN cells in PCOS. MiR-155-5p silencing attenuated glycolytic 
      activation in KGN cells; overexpression of miR-155-5p significantly promoted 
      glycolysis in KGN cells in PCOS. In this study, HK2 was found to be the mediator 
      of miR-143-3p and miR-155-5p in FF-derived exosome-mediated regulation of 
      glycolysis in KGN cells. Reduced glycolysis accelerated apoptosis of KGN cells, 
      which mediated follicular dysplasia through ATP, lactate and apoptotic pathways. 
      CONCLUSIONS: In conclusion, these results indicate that miR-143-3p and miR-155-5p 
      in FF-derived exosomes antagonistically regulate glycolytic-mediated follicular 
      dysplasia of GCs in PCOS. Video Abstract.
CI  - (c) 2022. The Author(s).
FAU - Cao, Jianping
AU  - Cao J
AD  - Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Health, 
      Guilin Medical University, Guilin, 541199, China.
AD  - State Key Laboratory for Conversation and Utilization of Subtropical 
      Agro-Bioresources, Guangxi University, Nanning, 530004, Guangxi, China.
FAU - Huo, Peng
AU  - Huo P
AD  - Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Health, 
      Guilin Medical University, Guilin, 541199, China.
FAU - Cui, Kuiqing
AU  - Cui K
AD  - State Key Laboratory for Conversation and Utilization of Subtropical 
      Agro-Bioresources, Guangxi University, Nanning, 530004, Guangxi, China.
FAU - Wei, Huimei
AU  - Wei H
AD  - Department of Reproductive Medical Center, The Affiliated Hospital of Guilin 
      Medical University, Guilin, 541001, China.
FAU - Cao, Junna
AU  - Cao J
AD  - Department of Reproductive Medical Center, The Affiliated Hospital of Guilin 
      Medical University, Guilin, 541001, China.
FAU - Wang, Jinyuan
AU  - Wang J
AD  - Department of Histology and Embryology, Clinical Anatomy and Reproductive 
      Medicine Application Institute, University of South China, Hengyang, 421001, 
      China.
FAU - Liu, Qingyou
AU  - Liu Q
AD  - State Key Laboratory for Conversation and Utilization of Subtropical 
      Agro-Bioresources, Guangxi University, Nanning, 530004, Guangxi, China.
FAU - Lei, Xiaocan
AU  - Lei X
AD  - Department of Histology and Embryology, Clinical Anatomy and Reproductive 
      Medicine Application Institute, University of South China, Hengyang, 421001, 
      China. 2019000013@usc.edu.cn.
FAU - Zhang, Shun
AU  - Zhang S
AD  - Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Health, 
      Guilin Medical University, Guilin, 541199, China. artzhangshun@glmc.edu.cn.
AD  - Department of Reproductive Medical Center, The Affiliated Hospital of Guilin 
      Medical University, Guilin, 541001, China. artzhangshun@glmc.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Video-Audio Media
DEP - 20220509
PL  - England
TA  - Cell Commun Signal
JT  - Cell communication and signaling : CCS
JID - 101170464
RN  - 0 (Lactates)
RN  - 0 (MIRN143 microRNA, human)
RN  - 0 (MIRN155 microRNA, human)
RN  - 0 (MicroRNAs)
SB  - IM
EIN - Cell Commun Signal. 2022 Aug 1;20(1):116. PMID: 35915462
MH  - Cell Proliferation
MH  - Female
MH  - Follicular Fluid/metabolism
MH  - Glycolysis
MH  - Granulosa Cells/metabolism/pathology
MH  - Humans
MH  - Lactates/metabolism
MH  - *MicroRNAs/genetics/metabolism
MH  - *Polycystic Ovary Syndrome/genetics/metabolism/pathology
PMC - PMC9082924
OTO - NOTNLM
OT  - Exosomes
OT  - Glycolysis
OT  - HK2
OT  - Polycystic ovary syndrome
OT  - miR-143-3p
OT  - miR-155-5p
COIS- None.
EDAT- 2022/05/10 06:00
MHDA- 2022/05/12 06:00
PMCR- 2022/05/09
CRDT- 2022/05/09 23:37
PHST- 2022/01/18 00:00 [received]
PHST- 2022/04/02 00:00 [accepted]
PHST- 2022/05/09 23:37 [entrez]
PHST- 2022/05/10 06:00 [pubmed]
PHST- 2022/05/12 06:00 [medline]
PHST- 2022/05/09 00:00 [pmc-release]
AID - 10.1186/s12964-022-00876-6 [pii]
AID - 876 [pii]
AID - 10.1186/s12964-022-00876-6 [doi]
PST - epublish
SO  - Cell Commun Signal. 2022 May 9;20(1):61. doi: 10.1186/s12964-022-00876-6.