MicroRNA-214-3p protects against myocardial ischemia-reperfusion injury by targeting demethylase lysine demethylase 3A.
Apoptosis
Inflammatory response
Lysine demethylase 3A
MicroRNA-214-3p
Myocardial ischemia-reperfusion injury
Oxidative tress
Journal
Regenerative therapy
ISSN: 2352-3204
Titre abrégé: Regen Ther
Pays: Netherlands
ID NLM: 101709085
Informations de publication
Date de publication:
Jun 2023
Jun 2023
Historique:
received:
09
06
2022
revised:
12
01
2023
accepted:
26
01
2023
medline:
5
4
2023
entrez:
4
4
2023
pubmed:
5
4
2023
Statut:
epublish
Résumé
Many studies have explored the roles of microRNAs (miRs) in myocardial ischemia/reperfusion injury (MI/RI), while the function of miR-214-3p in MI/RI remained obscure. This study aims to unravel the regulatory mechanism of miR-214-3p in MI/RI via targeting histone demethylase lysine demethylase 3A (KDM3A). MI/RI rat model was established by ligating the left anterior descending coronary artery. MiR-214-3p and KDM3A expression in myocardial tissues of MI/RI rats was examined. Then, the serum oxidative stress factors, inflammatory factors, pathological changes of myocardial tissues, cardiomyocyte apoptosis, and fibrosis of myocardial tissues were detected in MI/RI rats intervening with miR-214-3p or KDM3A expression. The targeting relation between miR-214-3p and KDM3A was validated. MiR-214-3p was low-expressed while KDM3A was high-expressed in MI/RI rat model. Up-regulated miR-214-3p or down-regulated KDM3A protected against MI/RI via mitigating serum oxidative response, reducing the levels of inflammatory factors, alleviating the pathological changes of myocardial tissues, and decreasing cardiomyocyte apoptosis and fibrosis of myocardial tissue. KDM3A amplification reversed the therapeutic effects of elevated miR-214-3p on MI/RI. KDM3A was targeted by miR-214-3p. miR-214-3p hinders cardiomyocyte apoptosis and myocardial injury in MI/RI rats via regulating KDM3A. Thus, miR-214-3p may function as a potential candidate for MI/RI treatment.
Identifiants
pubmed: 37013195
doi: 10.1016/j.reth.2023.01.008
pii: S2352-3204(23)00008-1
pmc: PMC10066509
doi:
Types de publication
Journal Article
Langues
eng
Pagination
17-24Informations de copyright
© 2023, The Japanese Society for Regenerative Medicine. Production and hosting by Elsevier B.V.
Déclaration de conflit d'intérêts
The authors declare no conflicts of interest.
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