PMID- 33250684
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201201
IS  - 1611-2156 (Print)
IS  - 1611-2156 (Electronic)
IS  - 1611-2156 (Linking)
VI  - 19
DP  - 2020
TI  - Circ_0010729 knockdown protects cardiomyocytes against hypoxic dysfunction via 
      miR-370-3p/TRAF6 axis.
PG  - 1520-1532
LID - 10.17179/excli2020-2809 [doi]
AB  - Few studies have addressed the mechanism by which circ_0010729 regulates 
      hypoxia-induced cell injury in cardiovascular diseases. However, its role and its 
      regulatory mechanism in myocardial infarction remain to be explored. Cell 
      viability, cycle, apoptosis, and migration were analyzed using cell counting 
      kit-8 assay, flow cytometry, caspase-3 activity assay kit and transwell assay, 
      respectively. Tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6) 
      concentrations were examined by enzyme-linked immunosorbent assay. Glucose 
      metabolism was calculated by detecting ATP production, glucose uptake and lactate 
      production. Levels of circ_0010729, miR-370-3p and TNF Receptor Associated Factor 
      6 (TRAF6) were detected using quantitative real-time polymerase chain reaction or 
      western blot. The direct interaction between circ_0010729 and TRAF6 or miR-370-3p 
      was verified using dual-luciferase reporter assay and RNA immunoprecipitation 
      assay. Under hypoxia condition, cardiomyocytes suffered from cell viability 
      suppression, cell cycle arrest, cell apoptosis promotion, migration reduction, 
      increase of inflammatory factor IL-6 and TNF-alpha, as well as glycolysis inhibition. 
      Circ_0010729 expression was up-regulated in the cardiomyocytes at different 
      hypoxia-exposed time points. Circ_0010729 knockdown protected cardiomyocytes 
      against hypoxic dysfunction, while circ_0010729 overexpression showed inverse 
      effects. MiR-370-3p was confirmed to directly bind to circ_0010729 or TRAF6. 
      MiR-370-3p inhibition attenuated the protective effects of circ_0010729 knockdown 
      on hypoxia-modulated cardiomyocyte dysfunction. MiR-370-3p restoration protected 
      cardiomyocytes against hypoxic injury via targeting TRAF6. Besides, circ_0010729 
      indirectly regulated TRAF6 expression via miR-370-3p. This study demonstrated 
      that circ_0010729 knockdown attenuated hypoxia-induced cardiomyocyte dysfunction 
      via miR-370-3p/TRAF6 axis, indicating a potential therapeutic target for 
      myocardial infarction.
CI  - Copyright (c) 2020 Zhang et al.
FAU - Zhang, Jingjing
AU  - Zhang J
AD  - Coronary Care Unit, Department of Cardiology, People's Hospital of Zhengzhou 
      University, Zhengzhou City, Henan Procince, China.
FAU - Gao, Chuanyu
AU  - Gao C
AD  - Department of Cardiology, People's Hospital of Zhengzhou University, Zhengzhou 
      City, Henan Procince, China.
FAU - Zhang, Jing
AU  - Zhang J
AD  - Coronary Care Unit, Department of Cardiology, People's Hospital of Zhengzhou 
      University, Zhengzhou City, Henan Procince, China.
FAU - Ye, Famin
AU  - Ye F
AD  - Coronary Care Unit, Department of Cardiology, People's Hospital of Zhengzhou 
      University, Zhengzhou City, Henan Procince, China.
LA  - eng
PT  - Journal Article
DEP - 20201111
PL  - Germany
TA  - EXCLI J
JT  - EXCLI journal
JID - 101299402
PMC - PMC7689242
OTO - NOTNLM
OT  - TRAF6
OT  - cardiomyocytes
OT  - circ_0010729
OT  - hypoxia
OT  - miR-370-3p
EDAT- 2020/12/01 06:00
MHDA- 2020/12/01 06:01
PMCR- 2020/11/11
CRDT- 2020/11/30 05:52
PHST- 2020/08/19 00:00 [received]
PHST- 2020/10/21 00:00 [accepted]
PHST- 2020/11/30 05:52 [entrez]
PHST- 2020/12/01 06:00 [pubmed]
PHST- 2020/12/01 06:01 [medline]
PHST- 2020/11/11 00:00 [pmc-release]
AID - 2020-2809 [pii]
AID - Doc1520 [pii]
AID - 10.17179/excli2020-2809 [doi]
PST - epublish
SO  - EXCLI J. 2020 Nov 11;19:1520-1532. doi: 10.17179/excli2020-2809. eCollection 
      2020.