Inhibition of miR-322-5p Protects Cardiac Myoblast Cells Against Hypoxia-Induced Apoptosis and Injury Through Regulating CIAPIN1.
Animals
Apoptosis
Apoptosis Regulatory Proteins
/ genetics
Cell Hypoxia
Cell Line
MicroRNAs
/ genetics
Myoblasts, Cardiac
/ metabolism
Myocytes, Cardiac
/ metabolism
Oligonucleotides, Antisense
/ genetics
Phosphatidylinositol 3-Kinase
/ metabolism
Proto-Oncogene Proteins c-akt
/ metabolism
RNA Interference
RNA, Small Interfering
/ genetics
Rats, Sprague-Dawley
Signal Transduction
Journal
Journal of cardiovascular pharmacology
ISSN: 1533-4023
Titre abrégé: J Cardiovasc Pharmacol
Pays: United States
ID NLM: 7902492
Informations de publication
Date de publication:
01 02 2021
01 02 2021
Historique:
received:
03
08
2020
accepted:
15
10
2020
entrez:
4
2
2021
pubmed:
5
2
2021
medline:
15
12
2021
Statut:
ppublish
Résumé
Hypoxia leads to insufficient supply of blood and nutrients, which is major incentive for cardiomyocyte injury and apoptosis. Previous studies reported the regulation effects of microRNAs (miRNAs) in myocardial infarction, whereas function and molecular mechanisms of miR-322-5p were still unclear. Therefore, our study focused on the biological role of miR-322-5p in hypoxia-induced cardiac myoblast cells apoptosis and injury. The expression levels of miR-322-5p and cytokine-induced apoptosis inhibitor 1 (CIAPIN1) were measured by real-time quantitative polymerase chain reaction in cardiac myoblast cells. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide (MTT), lactic dehydrogenase, and flow cytometry assays were performed to examine proliferation, injury, and apoptosis of cardiac myoblast cells, respectively. The protein expression levels were evaluated with western blot assay. The relationship between miR-322-5p and CIAPIN1 was confirmed by dual-luciferase reporter analysis. We found that miR-322-5p level was increased in cardiac myoblast cells exposed to hypoxia. In addition, miR-322-5p silencing could weaken injury and apoptosis in cardiac myoblast cells induced by hypoxia; meanwhile, inhibition of miR-322-5p activation of phosphatidylinositol-3 kinases (PI3K)/protein kinase B (AKT) signal pathway. Besides, CIAPIN1 was a target mRNA of miR-322-5p based on bioinformatics prediction. CIAPIN1 knockdown reversed the effects of miR-322-5p silencing on hypoxic cardiac myoblast cells. Suppression of miR-322-5p protected cardiac myoblast cells against hypoxia-induced injury and apoptosis through regulation of CIAPIN1 expression and PI3K/AKT signal pathway.
Identifiants
pubmed: 33538533
doi: 10.1097/FJC.0000000000000949
pii: 00005344-202102000-00011
doi:
Substances chimiques
Apoptosis Regulatory Proteins
0
MIRN322 microRNA, rat
0
MicroRNAs
0
Oligonucleotides, Antisense
0
RNA, Small Interfering
0
cytokine-induced apoptosis inhibitor 1, rat
0
Phosphatidylinositol 3-Kinase
EC 2.7.1.137
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
200-207Informations de copyright
Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.
Déclaration de conflit d'intérêts
The authors report no conflicts of interest.
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