PMID- 29532993
OWN - NLM
STAT- MEDLINE
DCOM- 20191125
LR  - 20210719
IS  - 1582-4934 (Electronic)
IS  - 1582-1838 (Print)
IS  - 1582-1838 (Linking)
VI  - 22
IP  - 6
DP  - 2018 Jun
TI  - MicroRNA-30c suppresses the pro-fibrogenic effects of cardiac fibroblasts induced 
      by TGF-beta1 and prevents atrial fibrosis by targeting TGFbetaRII.
PG  - 3045-3057
LID - 10.1111/jcmm.13548 [doi]
AB  - Atrial fibrosis serves as an important contributor to atrial fibrillation (AF). 
      Recent data have suggested that microRNA-30c (miR-30c) is involved in fibrotic 
      remodelling and cancer development, but the specific role of miR-30c in atrial 
      fibrosis remains unclear. The purpose of this study was to investigate the role 
      of miR-30c in atrial fibrosis and its underlying mechanisms through in vivo and 
      in vitro experiments. Our results indicate that miR-30c is significantly 
      down-regulated in the rat abdominal aortic constriction (AAC) model and in the 
      cellular model of fibrosis induced by transforming growth factor-beta1 (TGF-beta1). 
      Overexpression of miR-30c in cardiac fibroblasts (CFs) markedly inhibits CF 
      proliferation, differentiation, migration and collagen production, whereas 
      decrease in miR-30c leads to the opposite results. Moreover, we identified 
      TGFbetaRII as a target of miR-30c. Finally, transferring adeno-associated virus 9 
      (AAV9)-miR-30c into the inferior vena cava of rats attenuated fibrosis in the 
      left atrium following AAC. These data indicate that miR-30c attenuates atrial 
      fibrosis via inhibition of CF proliferation, differentiation, migration and 
      collagen production by targeting TGFbetaRII, suggesting that miR-30c might be a 
      novel potential therapeutic target for preventing atrial fibrosis.
CI  - (c) 2018 The Authors. Journal of Cellular and Molecular Medicine published by John 
      Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
FAU - Xu, Juan
AU  - Xu J
AUID- ORCID: 0000-0002-2122-6469
AD  - Department of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong 
      University School of Medicine, Shanghai, China.
FAU - Wu, Haiqing
AU  - Wu H
AD  - Department of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong 
      University School of Medicine, Shanghai, China.
FAU - Chen, Songwen
AU  - Chen S
AD  - Department of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong 
      University School of Medicine, Shanghai, China.
FAU - Qi, Baozhen
AU  - Qi B
AD  - Department of Cardiology, Shanghai Institute of Cardiovascular Disease, Zhongshan 
      Hospital, Fudan University, Shanghai, China.
FAU - Zhou, Genqing
AU  - Zhou G
AD  - Department of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong 
      University School of Medicine, Shanghai, China.
FAU - Cai, Lidong
AU  - Cai L
AD  - Department of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong 
      University School of Medicine, Shanghai, China.
FAU - Zhao, Liqun
AU  - Zhao L
AD  - Department of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong 
      University School of Medicine, Shanghai, China.
FAU - Wei, Yong
AU  - Wei Y
AD  - Department of Cardiology, Shanghai Songjiang Central Hospital, Shanghai, China.
FAU - Liu, Shaowen
AU  - Liu S
AD  - Department of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong 
      University School of Medicine, Shanghai, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180313
PL  - England
TA  - J Cell Mol Med
JT  - Journal of cellular and molecular medicine
JID - 101083777
RN  - 0 (MIRN30 microRNA, rat)
RN  - 0 (MIRN30b microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (TGFB1 protein, human)
RN  - 0 (Transforming Growth Factor beta1)
RN  - EC 2.7.11.30 (Receptor, Transforming Growth Factor-beta Type II)
RN  - EC 2.7.11.30 (TGFBR2 protein, human)
SB  - IM
MH  - Animals
MH  - Atrial Fibrillation/*genetics/metabolism/pathology
MH  - Cell Differentiation/genetics
MH  - Cell Movement/genetics
MH  - Cell Proliferation/genetics
MH  - Fibrosis/*genetics/pathology
MH  - HEK293 Cells
MH  - Heart Atria/metabolism/pathology
MH  - Humans
MH  - MicroRNAs/*genetics
MH  - Myocardium/metabolism/pathology
MH  - Myofibroblasts/metabolism
MH  - Rats
MH  - Receptor, Transforming Growth Factor-beta Type II/*genetics
MH  - Transforming Growth Factor beta1/*genetics
PMC - PMC5980214
OTO - NOTNLM
OT  - TGFbetaRII
OT  - atrial fibrosis
OT  - miR-30c
EDAT- 2018/03/14 06:00
MHDA- 2019/11/26 06:00
PMCR- 2018/06/01
CRDT- 2018/03/14 06:00
PHST- 2017/06/22 00:00 [received]
PHST- 2017/12/29 00:00 [accepted]
PHST- 2018/03/14 06:00 [pubmed]
PHST- 2019/11/26 06:00 [medline]
PHST- 2018/03/14 06:00 [entrez]
PHST- 2018/06/01 00:00 [pmc-release]
AID - JCMM13548 [pii]
AID - 10.1111/jcmm.13548 [doi]
PST - ppublish
SO  - J Cell Mol Med. 2018 Jun;22(6):3045-3057. doi: 10.1111/jcmm.13548. Epub 2018 Mar 
      13.