LncRNA Peg13 Alleviates Myocardial Infarction/Reperfusion Injury through Regulating MiR-34a/Sirt1-Mediated Endoplasmic Reticulum Stress.
Int Heart J
; 65(3): 517-527, 2024.
Article
en En
| MEDLINE
| ID: mdl-38825496
ABSTRACT
Myocardial infarction/reperfusion (I/R) injury significantly impacts the health of older individuals. We confirmed that the level of lncRNA Peg13 was downregulated in I/R injury. However, the detailed function of Peg13 in myocardial I/R injury has not yet been explored.To detect the function of Peg13, in vivo model of I/R injury was constructed. RT-qPCR was employed to investigate RNA levels, and Western blotting was performed to assess levels of endoplasmic reticulum stress and apoptosis-associated proteins. EdU staining was confirmed to assess the cell proliferation.I/R therapy dramatically produced myocardial injury, increased the infarct area, and decreased the amount of Peg13 in myocardial tissues of mice. In addition, hypoxia/reoxygenation (H/R) notably induced the apoptosis and promoted the endoplasmic reticulum (ER) stress of HL-1 cells, while overexpression of Peg13 reversed these phenomena. Additionally, Peg13 may increase the level of Sirt1 through binding to miR-34a. Upregulation of Peg13 reversed H/R-induced ER stress via regulation of miR-34a/Sirt1 axis.LncRNA Peg13 reduces ER stress in myocardial infarction/reperfusion injury through mediation of miR-34a/Sirt1 axis. Hence, our research might shed new lights on developing new strategies for the treatment of myocardial I/R injury.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Daño por Reperfusión Miocárdica
/
MicroARNs
/
Sirtuina 1
/
Estrés del Retículo Endoplásmico
/
ARN Largo no Codificante
Límite:
Animals
Idioma:
En
Revista:
Int Heart J
Asunto de la revista:
CARDIOLOGIA
Año:
2024
Tipo del documento:
Article
Pais de publicación:
Japón