Article ; Online: Overexpression of microRNA-202-3p protects against myocardial ischemia-reperfusion injury through activation of TGF-β1/Smads signaling pathway by targeting TRPM6.
2019 Volume 18, Issue 5, Page(s) 621–637
Abstract: ... 202-3p) in regulating cardiomyocyte apoptosis, in respective of the TGF-β1/Smads signaling pathway ... of myocardial ischemic-reperfusion (I/R) injury. In this study, we explore the role and mechanism of microRNA-202-3p (miR ... suggest that miR-202-3p offers protection against ventricular remodeling after myocardial I/R injury via ...
| Abstract | MicroRNAs (miRNAs) have been found to act as key regulators in the pathogenesis of myocardial ischemic-reperfusion (I/R) injury. In this study, we explore the role and mechanism of microRNA-202-3p (miR-202-3p) in regulating cardiomyocyte apoptosis, in respective of the TGF-β1/Smads signaling pathway by targeting the transient receptor potential cation channel, subfamily M, member 6 (TRPM6). The targeting relationship between miR-202-3p and TRPM6 was verified by a dual-luciferase reporter gene assay. Sprague-Dawley rat models of myocardial I/R injury were initially established and treated with different mimics, inhibitors and siRNAs to test the effects of miR-202-3p and TRPM6 on myocardial I/R injury. The levels of inflammatory factors; IL-1β, IL-6, TNF-α as well as the degree of myocardial fibrosis and cardiomyocyte apoptosis were determined in rats transfected with different plasmids. TRPM6 was found to be the target of miR-202-3p. Up-regulated miR-202-3p or knockdown of TRPM-6 alleviated oxidative stress and inflammatory response, reduced ventricular mass, altered cardiac hemodynamics, suppressed myocardial infarction, attenuated cell apoptosis, and inhibited myocardial fibrosis. MiR-202-3p overexpression activates the TGF-β1/Smads signaling pathway by negatively regulating TRPM6 expression. Taken together, these findings suggest that miR-202-3p offers protection against ventricular remodeling after myocardial I/R injury via activation of the TGF-β1/Smads signaling pathway. |
|||||
|---|---|---|---|---|---|---|
| MeSH term(s) | Animals ; Antagomirs/metabolism ; Apoptosis ; Cytokines/metabolism ; Disease Models, Animal ; Male ; MicroRNAs/antagonists & inhibitors ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Myocardial Reperfusion Injury/metabolism ; Myocardial Reperfusion Injury/pathology ; Oxidative Stress ; RNA Interference ; RNA, Small Interfering/metabolism ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Smad Proteins/metabolism ; Superoxide Dismutase/metabolism ; TRPM Cation Channels/antagonists & inhibitors ; TRPM Cation Channels/genetics ; TRPM Cation Channels/metabolism ; Transforming Growth Factor beta1/metabolism ; Up-Regulation | |||||
| Chemical Substances | Antagomirs ; Cytokines ; MicroRNAs ; RNA, Small Interfering ; Smad Proteins ; TRPM Cation Channels ; TRPM6 protein, rat ; Transforming Growth Factor beta1 ; Superoxide Dismutase (EC 1.15.1.1) | |||||
| Language | English | |||||
| Publishing date | 2019-02-27 | |||||
| Publishing country | United States | |||||
| Document type | Journal Article ; Retracted Publication | |||||
| ZDB-ID | 2146183-1 | |||||
| ISSN | 1551-4005 ; 1538-4101 ; 1554-8627 | |||||
| ISSN (online) | 1551-4005 | |||||
| ISSN | 1538-4101 ; 1554-8627 | |||||
| DOI | 10.1080/15384101.2019.1580494 | |||||
| Shelf mark |
|
|||||
| Database | MEDical Literature Analysis and Retrieval System OnLINE |
Full text online
More links
Kategorien
In stock of ZB MED Cologne/Königswinter
| Zs.A 5881: Show issues | Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG) |
Order via subito
This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.