MiR-32-3p Regulates Myocardial Injury Induced by Microembolism and Microvascular Obstruction by Targeting RNF13 to Regulate the Stability of Atherosclerotic Plaques.
J Cardiovasc Transl Res
; 15(1): 143-166, 2022 02.
Article
em En
| MEDLINE
| ID: mdl-34185281
ABSTRACT
This study aimed to explore the molecular mechanism of myocardial protection. The effects of miR-32-3p and ring finger protein 13 (RNF13) on endoplasmic reticulum (ER) stress-induced apoptosis of A-10 cells and human umbilical vein endothelial cells (HUVEC) were detected using flow cytometry. The effects of miR-32-3p and phenylbutyric acid (PBA) on plaque instability and myocardial tissue injury in rats were investigated after establishment of arterial plaque model and embolization model and treatment with miR-32-3p-antagomir and PBA. RNF13, which was differentially expressed in myocardial infarction, was the direct target gene of miR-32-3p. MiR-32-3p inhibited RNF13 expression and targeted RNF13 to inhibit ER stress-induced cell apoptosis. Furthermore, inhibiting miR-32-3p expression induced arterial plaque instability by reducing survival, increasing pathological lesions in arterial tissue, up-regulating ER stress-related proteins, and regulating the expressions of apoptosis-related proteins in the model rats. However, PBA reversed the effects of miR-32-3p-antagomir on the model rats. MiR-32-3p regulates myocardial injury induced by micro-embolism and micro-vascular obstruction by targeting RNF13 to regulate the stability of atherosclerotic plaques.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
MicroRNAs
/
Ubiquitina-Proteína Ligases
/
Placa Aterosclerótica
/
Estresse do Retículo Endoplasmático
/
Infarto do Miocárdio
Tipo de estudo:
Prognostic_studies
Limite:
Animals
/
Humans
Idioma:
En
Revista:
J Cardiovasc Transl Res
Assunto da revista:
ANGIOLOGIA
/
CARDIOLOGIA
Ano de publicação:
2022
Tipo de documento:
Article
País de afiliação:
China