Cargando…

Protective effect of miR378* on doxorubicin‐induced cardiomyocyte injury via calumenin

Doxorubicin (Dox) is a highly effective antitumor antibiotic, however myocardial toxicity severely limits its use clinically. The pathogenesis of doxorubicin‐induced cardiomyopathy is unclear. In Dox cardiomyopathy mice, there is a decline in cardiac function, a change in myocardial pathology and a...

Descripción completa

Detalles Bibliográficos
Autores principales: Wang, Yu, Cui, Xiaoxue, Wang, Yilin, Fu, Yao, Guo, Xin, Long, Jie, Wei, Chengxi, Zhao, Ming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6055600/
https://www.ncbi.nlm.nih.gov/pubmed/29665007
http://dx.doi.org/10.1002/jcp.26615
_version_ 1783341205306736640
author Wang, Yu
Cui, Xiaoxue
Wang, Yilin
Fu, Yao
Guo, Xin
Long, Jie
Wei, Chengxi
Zhao, Ming
author_facet Wang, Yu
Cui, Xiaoxue
Wang, Yilin
Fu, Yao
Guo, Xin
Long, Jie
Wei, Chengxi
Zhao, Ming
author_sort Wang, Yu
collection PubMed
description Doxorubicin (Dox) is a highly effective antitumor antibiotic, however myocardial toxicity severely limits its use clinically. The pathogenesis of doxorubicin‐induced cardiomyopathy is unclear. In Dox cardiomyopathy mice, there is a decline in cardiac function, a change in myocardial pathology and a reduction in miR378* expression. Expression changes in calumenin, an endoplasmic reticulum stress (ERS) chaperone protein and pathway factor, as well as apoptosis, were observed in cardiomyocytes after doxorubicin‐induced injury. However, miR378* increased calumenin expression, eased ERS, and reduced cardiomyocyte apoptosis, while, silencing miR378* reduced calumenin expression, aggravated ERS, and increased cardiomyocyte apoptosis. The above results indicate that miR378* alleviates ERS and inhibits the activation of the ERS‐mediated apoptosis signaling pathway in cardiomyocytes via regulating calumenin expression, thereby reducing cardiomyocyte apoptosis after doxorubicin‐induced injury. Increasing miR378* expression may be a new way to improve cardiac function and quality of life in patients with Dox cardiomyopathy.
format Online
Article
Text
id pubmed-6055600
institution National Center for Biotechnology Information
language English
publishDate 2018
publisher John Wiley and Sons Inc.
record_format MEDLINE/PubMed
spelling pubmed-60556002018-07-23 Protective effect of miR378* on doxorubicin‐induced cardiomyocyte injury via calumenin Wang, Yu Cui, Xiaoxue Wang, Yilin Fu, Yao Guo, Xin Long, Jie Wei, Chengxi Zhao, Ming J Cell Physiol Rapid Communications Doxorubicin (Dox) is a highly effective antitumor antibiotic, however myocardial toxicity severely limits its use clinically. The pathogenesis of doxorubicin‐induced cardiomyopathy is unclear. In Dox cardiomyopathy mice, there is a decline in cardiac function, a change in myocardial pathology and a reduction in miR378* expression. Expression changes in calumenin, an endoplasmic reticulum stress (ERS) chaperone protein and pathway factor, as well as apoptosis, were observed in cardiomyocytes after doxorubicin‐induced injury. However, miR378* increased calumenin expression, eased ERS, and reduced cardiomyocyte apoptosis, while, silencing miR378* reduced calumenin expression, aggravated ERS, and increased cardiomyocyte apoptosis. The above results indicate that miR378* alleviates ERS and inhibits the activation of the ERS‐mediated apoptosis signaling pathway in cardiomyocytes via regulating calumenin expression, thereby reducing cardiomyocyte apoptosis after doxorubicin‐induced injury. Increasing miR378* expression may be a new way to improve cardiac function and quality of life in patients with Dox cardiomyopathy. John Wiley and Sons Inc. 2018-04-17 2018-10 /pmc/articles/PMC6055600/ /pubmed/29665007 http://dx.doi.org/10.1002/jcp.26615 Text en © 2018 The Authors. Journal of Cellular Physiology Published by Wiley Periodicals, Inc. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Rapid Communications
Wang, Yu
Cui, Xiaoxue
Wang, Yilin
Fu, Yao
Guo, Xin
Long, Jie
Wei, Chengxi
Zhao, Ming
Protective effect of miR378* on doxorubicin‐induced cardiomyocyte injury via calumenin
title Protective effect of miR378* on doxorubicin‐induced cardiomyocyte injury via calumenin
title_full Protective effect of miR378* on doxorubicin‐induced cardiomyocyte injury via calumenin
title_fullStr Protective effect of miR378* on doxorubicin‐induced cardiomyocyte injury via calumenin
title_full_unstemmed Protective effect of miR378* on doxorubicin‐induced cardiomyocyte injury via calumenin
title_short Protective effect of miR378* on doxorubicin‐induced cardiomyocyte injury via calumenin
title_sort protective effect of mir378* on doxorubicin‐induced cardiomyocyte injury via calumenin
topic Rapid Communications
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6055600/
https://www.ncbi.nlm.nih.gov/pubmed/29665007
http://dx.doi.org/10.1002/jcp.26615
work_keys_str_mv AT wangyu protectiveeffectofmir378ondoxorubicininducedcardiomyocyteinjuryviacalumenin
AT cuixiaoxue protectiveeffectofmir378ondoxorubicininducedcardiomyocyteinjuryviacalumenin
AT wangyilin protectiveeffectofmir378ondoxorubicininducedcardiomyocyteinjuryviacalumenin
AT fuyao protectiveeffectofmir378ondoxorubicininducedcardiomyocyteinjuryviacalumenin
AT guoxin protectiveeffectofmir378ondoxorubicininducedcardiomyocyteinjuryviacalumenin
AT longjie protectiveeffectofmir378ondoxorubicininducedcardiomyocyteinjuryviacalumenin
AT weichengxi protectiveeffectofmir378ondoxorubicininducedcardiomyocyteinjuryviacalumenin
AT zhaoming protectiveeffectofmir378ondoxorubicininducedcardiomyocyteinjuryviacalumenin