Role of PNPT1 in cardiomyocyte apoptosis induced by oxygen-glucose deprivation.
10.12122/j.issn.1673-4254.2022.04.15
- Author:
Xin Qin ZHANG
1
;
Xiong WANG
2
;
Qin LI
3
;
Ying Mei CHEN
2
;
Xin Yan ZHANG
4
;
Peng WANG
2
;
Mu YUAN
5
;
Hai Feng PEI
1
Author Information
1. College of Medicine, Southwest Jiaotong University, Chengdu 611756, China.
2. Department of Cardiology, General Hospital of Western Theater Command, Chengdu 610083, China.
3. Second Ward of Cadres, General Hospital of Western Theater Command, Chengdu 610083, China.
4. Medical Information Data Office, General Hospital of Western Theater Command, Chengdu 610083, China.
5. Medical Center, General Hospital of Western Theater Command, Chengdu 610083, China.
- Publication Type:Journal Article
- Keywords:
apoptosis-related mRNA degradation;
myocardial cell apoptosis;
oxygen-glucose deprivation;
polyribonucleotide nucleotidyl-transferase 1
- MeSH:
Animals;
Apoptosis;
Cell Survival;
Glucose/pharmacology*;
Mice;
Myocytes, Cardiac;
Oxygen/metabolism*;
RNA, Messenger/metabolism*;
RNA, Small Interfering/metabolism*
- From:
Journal of Southern Medical University
2022;42(4):584-590
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the effect of inhibiting polyribonucleotide nucleotidyl-transferase 1 (PNPT1) on oxygen-glucose deprivation (OGD)-induced apoptosis of mouse atrial myocytes.
METHODS:Cultured mouse atrial myocytes (HL-1 cells) with or without OGD were transfected with PNPT1-siRNA or a negative control siRNA (NC-siRNA group), and the cell survival rate was detected using CCK-8 assay. The expression levels of ACTB and TUBA mRNA were detected with qPCR, and the protein expression of PNPT1 was detected with Western blotting. The apoptosis rate of the treated cells was determined with flow cytometry, the mitochondrial membrane potential was detected using JC-1 kit, and the mitochondrial morphology was observed using transmission electron microscope.
RESULTS:With the extension of OGD time, the protein expression levels of PNPT1 increased progressively in the cytoplasm of HL-1 cells (P < 0.05). Transfection with PNPT1-siRNA significantly reduced PNPT1 expression in HL-1 cells (P < 0.05). Exposure to OGD significantly enhanced degradation of ACTB and TUBA mRNA (P < 0.05) and markedly increased the apoptosis rate of HL-1 cells (P < 0.05), and these changes were significantly inhibited by transfection with PNPT1-siRNA (P < 0.05), which obviously increased mitochondrial membrane potential and improved mitochondrial morphology of HL-1 cells exposed to OGD.
CONCLUSION:Inhibition of PNPT1 improves mitochondrial damage and reduces degradation of apoptotic-associated mRNAs to alleviate OGD-induced apoptosis of mouse atrial myocyte.
