Cardiomyocyte pyroptosis inhibited by dental pulp-derived mesenchymal stem cells via the miR-19a-3p/IRF-8/MAPK pathway in ischemia-reperfusion.
10.1097/CM9.0000000000003623
- Author:
Yi LI
1
;
Xiang WANG
1
;
Sixian WENG
1
;
Chenxi XIA
1
;
Xuyang MENG
1
;
Chenguang YANG
1
;
Ying GUO
1
;
Zuowei PEI
2
;
Haiyang GAO
1
;
Fang WANG
1
Author Information
1. Department of Cardiology, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing 100730, China.
2. Department of Cardiology, Central Hospital of Dalian University of Technology, Dalian, Liaoning 116089, China.
- Publication Type:Journal Article
- Keywords:
Acute myocardial infarction;
Dental pulp-derived;
IRF-8;
Interferon regulatory factor 8;
Ischemia–reperfusion;
MAPK;
Mesenchymal stem cells;
MiR-19a-3p;
Mitogen-activated protein kinase;
Pyroptosis
- MeSH:
Animals;
MicroRNAs/metabolism*;
Pyroptosis/genetics*;
Mesenchymal Stem Cells/metabolism*;
Myocytes, Cardiac/cytology*;
Mice;
Male;
Mice, Inbred C57BL;
Dental Pulp/cytology*;
Myocardial Reperfusion Injury/therapy*;
MAP Kinase Signaling System/physiology*
- From:
Chinese Medical Journal
2025;138(18):2336-2346
- CountryChina
- Language:English
-
Abstract:
BACKGROUND:The protective effect of mesenchymal stem cells (MSCs) on cardiac ischemia-reperfusion (I/R) injury has been widely reported. Dental pulp-derived mesenchymal stem cells (DP-MSCs) have therapeutic effects on various diseases, including diabetes and cirrhosis. This study aimed to determine the therapeutic effects of DP-MSCs on I/R injury and elucidate the underlying mechanism.
METHODS:Myocardial I/R injury model mice were treated with DP-MSCs or a miR-19a-3p mimic. The infarct volume, fibrotic area, pyroptosis, inflammation level, and cardiac function were measured. Cardiomyocytes exposed to hypoxia-reoxygenation were transfected with the miR-19a-3p mimic, miR-19a-3p inhibitor, or negative control. Pyroptosis and protein expression in the interferon regulatory factor 8/mitogen-activated protein kinase (IRF-8/MAPK) pathway were measured.
RESULTS:DP-MSCs protected cardiac function in cardiac I/R-injured mice and inhibited cardiomyocyte pyroptosis. The upregulation of miR-19a-3p protected cardiac function, inhibited cardiomyocyte pyroptosis, and inhibited IRF-8/MAPK signaling in cardiac I/R-injured mice. DP-MSCs inhibited cardiomyocyte pyroptosis and the IRF-8/MAPK signaling by upregulating the miR-19a-3p levels in cardiomyocytes injured by I/R.
CONCLUSION:DP-MSCs protected cardiac function by inhibiting cardiomyocyte pyroptosis through miR-19a-3p under I/R conditions.
