miR-362-3p Targets Orosomucoid 1 to Promote Cell Proliferation, Restrain Cell Apoptosis and Thereby Mitigate Hypoxia/Reoxygenation-Induced Cardiomyocytes Injury.


Journal

Cardiovascular toxicology
ISSN: 1559-0259
Titre abrégé: Cardiovasc Toxicol
Pays: United States
ID NLM: 101135818

Informations de publication

Date de publication:
05 2021
Historique:
received: 17 09 2020
accepted: 30 12 2020
pubmed: 19 1 2021
medline: 27 1 2022
entrez: 18 1 2021
Statut: ppublish

Résumé

This study aimed to investigate the mechanism of how miR-362-3p/orosomucoid 1 (ORM1) involved in hypoxia/reoxygenation (H/R)-induced cardiomyocytes injury. Based on data obtained from Gene Expression Omnibus (GEO) database, we revealed that ORM1 was highly expressed and positively correlated with the expression of inflammatory factors (MAPK1, MAPK3, IL1B and CASP9). miR-362-3p was identified as an upstream regulatory miRNA of ORM1 and negatively modulated the mRNA and protein expression levels of ORM1 in H/R-injured cardiomyocytes. Moreover, we found that miR-362-3p was downregulated in cardiomyocytes injured by H/R. The promoting influence of miR-362-3p mimic on the proliferation and the inhibitory effect of miR-362-3p mimic on the apoptosis of H/R-stimulated cardiomyocytes were eliminated by overexpression of ORM1. Furthermore, miR-362-3p affected the expression of MAPK1, MAPK3, IL1B and CASP9 in H/R-injured cardiomyocytes through targeting ORM1. Our outcomes illustrated that miR-362-3p exhibited a protective influence on H/R-induced cardiomyocytes through targeting ORM1.

Identifiants

pubmed: 33459949
doi: 10.1007/s12012-020-09631-0
pii: 10.1007/s12012-020-09631-0
doi:

Substances chimiques

IL1B protein, human 0
Interleukin-1beta 0
MIRN362 microRNA, human 0
MicroRNAs 0
ORM1 protein, human 0
Orosomucoid 0
MAPK1 protein, human EC 2.7.11.24
MAPK3 protein, human EC 2.7.11.24
Mitogen-Activated Protein Kinase 1 EC 2.7.11.24
Mitogen-Activated Protein Kinase 3 EC 2.7.11.24
CASP9 protein, human EC 3.4.22.-
Caspase 9 EC 3.4.22.-

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

387-398

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Auteurs

Meijing Shi (M)

School of Graduate, Hebei Medical University, Shijiazhuang, Hebei, 050017, P.R. China.

Xiuru Ma (X)

College of Integrated Chinese and Western Medicine, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, 050200, P.R. China.

Qian Yang (Q)

Department of Cardiology Center, Hebei General Hospital, No.348 Heping West Road, Shijiazhuang, Hebei, 050051, P.R. China.

Wenjing Wang (W)

Department of Cardiology Center, Hebei General Hospital, No.348 Heping West Road, Shijiazhuang, Hebei, 050051, P.R. China.

Xinning Li (X)

Department of Cardiology Center, Hebei General Hospital, No.348 Heping West Road, Shijiazhuang, Hebei, 050051, P.R. China.

Xuelian Song (X)

School of Graduate, Hebei Medical University, Shijiazhuang, Hebei, 050017, P.R. China.
Department of Cardiology Center, Hebei General Hospital, No.348 Heping West Road, Shijiazhuang, Hebei, 050051, P.R. China.

Yingxiao Li (Y)

Department of Cardiology Center, Hebei General Hospital, No.348 Heping West Road, Shijiazhuang, Hebei, 050051, P.R. China.

Yuetao Xie (Y)

Department of Cardiology Center, Hebei General Hospital, No.348 Heping West Road, Shijiazhuang, Hebei, 050051, P.R. China.

Yi Dang (Y)

Department of Cardiology Center, Hebei General Hospital, No.348 Heping West Road, Shijiazhuang, Hebei, 050051, P.R. China. dangyiemail@126.com.

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