PMID- 32844595
OWN - NLM
STAT- MEDLINE
DCOM- 20210506
LR  - 20210506
IS  - 1582-4934 (Electronic)
IS  - 1582-1838 (Print)
IS  - 1582-1838 (Linking)
VI  - 24
IP  - 19
DP  - 2020 Oct
TI  - Differentially expressed lnc-NOS2P3-miR-939-5p axis in chronic heart failure 
      inhibits myocardial and endothelial cells apoptosis via iNOS/TNFalpha pathway.
PG  - 11381-11396
LID - 10.1111/jcmm.15740 [doi]
AB  - Inflammatory cytokine-induced cell apoptosis is important for initiation and 
      progression of chronic heart failure (CHF). Non-coding RNAs, including long 
      non-coding RNAs and microRNAs, have emerged as critical regulators of this 
      pathological process. The role in regulating inflammation and induction to cell 
      apoptosis in CHF is not well understood. This study found CHF patients had 
      elevated serum miR-939-5p, with greater increase in New York Heart Association 
      (NYHA) I-II patients than in NYHA III-IV. Moreover, miR-939-5p was positively 
      correlated with B-type natriuretic peptide (BNP) in NYHA III-IV patients, while 
      not in NYHA I-II. Further study showed miR-939-5p mimics promoted cell 
      proliferation and inhibited inflammatory cytokine-induced apoptosis of HUVECs and 
      H9C2, while inhibition of endogenous miR-939-5p produced the opposite effects. 
      Induced nitric oxide synthase (iNOS) and tumour necrosis factor alpha (TNFalpha) were 
      identified as target genes of miR-939-5p. Additionally, lncRNA-NOS2P3 acted as an 
      endogenous sponge RNA to inhibit miR-939-5p expression, regulate the expression 
      of iNOS/TNFalpha and control inflammation-induced cells apoptosis. These suggest that 
      CHF patients exhibited elevated serum miR-939-5p level especially in NYHA I-II 
      grades. And lnc-NOS2P3-miR-939-5p-iNOS/TNFalpha pathway regulated inflammatory 
      cytokine-induced endothelial and myocardial cells apoptosis and provided a 
      promising strategy for diagnosis and treatment of CHF.
CI  - (c) 2020 The Authors. Journal of Cellular and Molecular Medicine published by 
      Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
FAU - Chen, Cuncun
AU  - Chen C
AUID- ORCID: 0000-0001-9473-7289
AD  - Department of Clinical Laboratory, Shanghai East Hospital, Tongji University 
      School of Medicine, Shanghai, China.
FAU - Zong, Ming
AU  - Zong M
AD  - Department of Clinical Laboratory, Shanghai East Hospital, Tongji University 
      School of Medicine, Shanghai, China.
FAU - Lu, Ying
AU  - Lu Y
AD  - Department of Clinical Laboratory, Shanghai East Hospital, Tongji University 
      School of Medicine, Shanghai, China.
FAU - Guo, Yide
AU  - Guo Y
AD  - Department of Clinical Laboratory, Shanghai East Hospital, Tongji University 
      School of Medicine, Shanghai, China.
FAU - Lv, Honggen
AU  - Lv H
AD  - Department of Clinical Laboratory, Shanghai East Hospital, Tongji University 
      School of Medicine, Shanghai, China.
FAU - Xie, Lihong
AU  - Xie L
AD  - Department of Clinical Laboratory, Shanghai East Hospital, Tongji University 
      School of Medicine, Shanghai, China.
FAU - Fu, Zhiyan
AU  - Fu Z
AD  - Department of Clinical Laboratory, Shanghai East Hospital, Tongji University 
      School of Medicine, Shanghai, China.
FAU - Cheng, Yu
AU  - Cheng Y
AD  - Department of Clinical Laboratory, Shanghai East Hospital, Tongji University 
      School of Medicine, Shanghai, China.
FAU - Si, Yuying
AU  - Si Y
AD  - Department of Clinical Laboratory, Shanghai East Hospital, Tongji University 
      School of Medicine, Shanghai, China.
FAU - Ye, Bei
AU  - Ye B
AD  - Department of Clinical Laboratory, Shanghai East Hospital, Tongji University 
      School of Medicine, Shanghai, China.
FAU - Fan, Lieying
AU  - Fan L
AD  - Department of Clinical Laboratory, Shanghai East Hospital, Tongji University 
      School of Medicine, Shanghai, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20200825
PL  - England
TA  - J Cell Mol Med
JT  - Journal of cellular and molecular medicine
JID - 101083777
RN  - 0 (Cytokines)
RN  - 0 (MIRN939 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
SB  - IM
MH  - *Apoptosis/genetics
MH  - Base Sequence
MH  - Chronic Disease
MH  - Cytokines/metabolism
MH  - *Gene Expression Regulation
MH  - Heart Failure/blood/*genetics
MH  - Human Umbilical Vein Endothelial Cells/metabolism/*pathology
MH  - Humans
MH  - Inflammation/genetics/pathology
MH  - MicroRNAs/blood/*genetics
MH  - Myocardium/*pathology
MH  - Nitric Oxide Synthase Type II/metabolism
MH  - RNA, Long Noncoding/*genetics/metabolism
MH  - *Signal Transduction
MH  - Tumor Necrosis Factor-alpha/metabolism
PMC - PMC7576245
OTO - NOTNLM
OT  - INOS
OT  - LncRNA-NOS2P3
OT  - TNFalpha
OT  - apoptosis
OT  - chronic heart failure
OT  - microRNA-939-5p
COIS- The authors confirm that there are no conflicts of interest.
EDAT- 2020/08/28 06:00
MHDA- 2021/05/07 06:00
PMCR- 2020/10/01
CRDT- 2020/08/27 06:00
PHST- 2019/09/29 00:00 [received]
PHST- 2020/07/06 00:00 [revised]
PHST- 2020/07/30 00:00 [accepted]
PHST- 2020/08/28 06:00 [pubmed]
PHST- 2021/05/07 06:00 [medline]
PHST- 2020/08/27 06:00 [entrez]
PHST- 2020/10/01 00:00 [pmc-release]
AID - JCMM15740 [pii]
AID - 10.1111/jcmm.15740 [doi]
PST - ppublish
SO  - J Cell Mol Med. 2020 Oct;24(19):11381-11396. doi: 10.1111/jcmm.15740. Epub 2020 
      Aug 25.