MiR-486 regulates cardiomyocyte apoptosis by p53-mediated BCL-2 associated mitochondrial apoptotic pathway
Abstract Background Cardiomyocyte apoptosis is a common pathological manifestation that occurs in several heart diseases. This study aimed to explore the mechanism of microRNA-486 (miR-486) in cardiomyocyte apoptosis by interfering with the p53-activated BCL-2 associated mitochondrial pathway. Metho...
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doaj-23a9d722fa3f41cbb83fdc6ae17606c72020-11-25T02:36:40ZengBMCBMC Cardiovascular Disorders1471-22612017-05-0117111210.1186/s12872-017-0549-7MiR-486 regulates cardiomyocyte apoptosis by p53-mediated BCL-2 associated mitochondrial apoptotic pathwayYuhan Sun0Qiang Su1Lang Li2Xiantao Wang3Yuanxi Lu4Jiabao Liang5Department of Cardiology, The First Affiliated Hospital of Guangxi Medical UniversityDepartment of Cardiology, The First Affiliated Hospital of Guangxi Medical UniversityDepartment of Cardiology, The First Affiliated Hospital of Guangxi Medical UniversityDepartment of Cardiology, The First Affiliated Hospital of Guangxi Medical UniversityDepartment of Cardiology, The First Affiliated Hospital of Guangxi Medical UniversityDepartment of Cardiology, The First Affiliated Hospital of Guangxi Medical UniversityAbstract Background Cardiomyocyte apoptosis is a common pathological manifestation that occurs in several heart diseases. This study aimed to explore the mechanism of microRNA-486 (miR-486) in cardiomyocyte apoptosis by interfering with the p53-activated BCL-2 associated mitochondrial pathway. Methods miR-486 mimics and inhibitors were transfected into the primary cardiomyocytes of suckling Sprague-Dawley rat pups, and H2O2 was used to induce apoptosis. Flow cytometry and TUNEL were both used to detect cardiomyocyte apoptosis, while the relative mRNA transcript and protein levels of miR-486, p53, Bbc3, BCL-2, and cleaved caspase-3 were detected using RT-PCR and western blot analysis, respectively. Results miR-486 overexpression significantly decreased the expressions of p53, Bbc3 and cleaved caspase-3 (P < 0.05), and BCL-2 expression was significantly increased (P < 0.05), which in turn caused a significant decrease in the rate of cardiomyocyte apoptosis (P < 0.05). In contrast, miR-486 silencing resulted in an elevated rate of cardiomyocyte apoptosis (P < 0.05). Conclusion miR-486 may regulate cardiomyocyte apoptosis via p53-mediated BCL-2 associated mitochondrial apoptotic pathway. Therefore, up-regulating miR-486 expression in cardiomyocytes can effectively reduce the activation of the BCL-2 associated mitochondrial apoptotic pathway, consequently protecting cardiomyocytes.http://link.springer.com/article/10.1186/s12872-017-0549-7CardiomyocyteApoptosismiR-486P53BCL-2 pathway |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Yuhan Sun Qiang Su Lang Li Xiantao Wang Yuanxi Lu Jiabao Liang |
spellingShingle |
Yuhan Sun Qiang Su Lang Li Xiantao Wang Yuanxi Lu Jiabao Liang MiR-486 regulates cardiomyocyte apoptosis by p53-mediated BCL-2 associated mitochondrial apoptotic pathway BMC Cardiovascular Disorders Cardiomyocyte Apoptosis miR-486 P53 BCL-2 pathway |
author_facet |
Yuhan Sun Qiang Su Lang Li Xiantao Wang Yuanxi Lu Jiabao Liang |
author_sort |
Yuhan Sun |
title |
MiR-486 regulates cardiomyocyte apoptosis by p53-mediated BCL-2 associated mitochondrial apoptotic pathway |
title_short |
MiR-486 regulates cardiomyocyte apoptosis by p53-mediated BCL-2 associated mitochondrial apoptotic pathway |
title_full |
MiR-486 regulates cardiomyocyte apoptosis by p53-mediated BCL-2 associated mitochondrial apoptotic pathway |
title_fullStr |
MiR-486 regulates cardiomyocyte apoptosis by p53-mediated BCL-2 associated mitochondrial apoptotic pathway |
title_full_unstemmed |
MiR-486 regulates cardiomyocyte apoptosis by p53-mediated BCL-2 associated mitochondrial apoptotic pathway |
title_sort |
mir-486 regulates cardiomyocyte apoptosis by p53-mediated bcl-2 associated mitochondrial apoptotic pathway |
publisher |
BMC |
series |
BMC Cardiovascular Disorders |
issn |
1471-2261 |
publishDate |
2017-05-01 |
description |
Abstract Background Cardiomyocyte apoptosis is a common pathological manifestation that occurs in several heart diseases. This study aimed to explore the mechanism of microRNA-486 (miR-486) in cardiomyocyte apoptosis by interfering with the p53-activated BCL-2 associated mitochondrial pathway. Methods miR-486 mimics and inhibitors were transfected into the primary cardiomyocytes of suckling Sprague-Dawley rat pups, and H2O2 was used to induce apoptosis. Flow cytometry and TUNEL were both used to detect cardiomyocyte apoptosis, while the relative mRNA transcript and protein levels of miR-486, p53, Bbc3, BCL-2, and cleaved caspase-3 were detected using RT-PCR and western blot analysis, respectively. Results miR-486 overexpression significantly decreased the expressions of p53, Bbc3 and cleaved caspase-3 (P < 0.05), and BCL-2 expression was significantly increased (P < 0.05), which in turn caused a significant decrease in the rate of cardiomyocyte apoptosis (P < 0.05). In contrast, miR-486 silencing resulted in an elevated rate of cardiomyocyte apoptosis (P < 0.05). Conclusion miR-486 may regulate cardiomyocyte apoptosis via p53-mediated BCL-2 associated mitochondrial apoptotic pathway. Therefore, up-regulating miR-486 expression in cardiomyocytes can effectively reduce the activation of the BCL-2 associated mitochondrial apoptotic pathway, consequently protecting cardiomyocytes. |
topic |
Cardiomyocyte Apoptosis miR-486 P53 BCL-2 pathway |
url |
http://link.springer.com/article/10.1186/s12872-017-0549-7 |
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