MicroRNA2213p contributes to cardiomyocyte injury in H2O2treated H9c2 cells and a rat model of myocardial ischemiareperfusion by targeting p57.
Int J Mol Med
; 42(1): 589-596, 2018 Jul.
Article
em En
| MEDLINE
| ID: mdl-29693157
ABSTRACT
Myocardial ischemiareperfusion (I/R) injury is a major cause of cardiovascular disease worldwide, and microRNAs have been implicated in the regulation of pathological and physiological processes in myocardial I/R injury. The present study aimed to investigate the role of microRNA (miR)2213p in myocardial I/R injury. Cell death and lactate dehydrogenase (LDH) activity were increased in hydrogen peroxide (H2O2)treated H9c2 cells, as measured by flow cytometry and an LDH detection kit. The expression of miR2213p was elevated in H2O2incubated cells and in remote areas of the rat I/R model, examined using reverse transcriptionquantitative polymerase chain reaction analysis. The overexpression of miR2213p enhanced the number of propidium iodide (PI)+ cells and the activity of LDH in H2O2treated cells. In I/Rinduced rats, the overexpression of miR2213p promoted the number of myosin+ cells and inhibited the fractional shortening of left ventricular diameter (FSLVD%). The results showed that the expression of p57 at the gene and protein levels was decreased in H9c2 cells incubated with H2O2 and in rats subjected to I/R surgery; the expression of p57 decreased following the overexpression of miR2213p. Subsequently, the hypothesis that p57 was the direct target of miR2213p was confirmed by performing a dualluciferase reporter assay. Finally, to examine the function of p57 in myocardial impairment, p57 was transfected into H9c2 cells and administered to the rats prior to undergoing H2O2 treatment and I/R surgery, respectively. The results indicated that p57 attenuated the number of PI+ cells and the activity of LDH in H2O2treated cells, whereas p57 downregulated the number of myosin+ cells and upregulated FSLVD% in the I/Rtreated rats. Therefore, these findings suggested that miR2213p exacerbated the H2O2induced myocardial damage in H9c2 cells and myocardial I/R injury in the rat model by modulating p57.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Traumatismo por Reperfusão Miocárdica
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Miócitos Cardíacos
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MicroRNAs
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Inibidor de Quinase Dependente de Ciclina p57
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Peróxido de Hidrogênio
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article