title: miR-19b controls cardiac fibroblast proliferation and migration.
abstract: Cardiac fibrosis is a fundamental constituent of a variety of cardiac dysfunction, making it a leading cause of death worldwide. However, no effective treatment for cardiac fibrosis is available. Therefore, novel therapeutics for cardiac fibrosis are highly needed. Recently, miR-19b has been found to be able to protect hydrogen peroxide (H2 O2 )-induced apoptosis and improve cell survival in H9C2 cardiomyocytes, while down-regulation of miR-19b had opposite effects, indicating that increasing miR-19b may be a new therapeutic strategy for attenuating cellular apoptosis during myocardial ischaemia-reperfusion injury. However, considering the fact that microRNAs might exert a cell-specific role, it is highly interesting to determine the role of miR-19b in cardiac fibroblasts. Here, we found that miR-19b was able to promote cardiac fibroblast proliferation and migration. However, miR-19b mimics and inhibitors did not modulate the expression level of collagen I. Pten was identified as a target gene of miR-19b, which was responsible for the effect of miR-19b in controlling cardiac fibroblast proliferation and migration. Our data suggest that the role of miR-19b is cell specific, and systemic miR-19b targeting in cardiac remodelling might be problematic. Therefore, it is highly needed and also urgent to investigate the role of miR-19b in cardiac remodelling in vivo.
authors.affiliation: Department of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital of NanTong University, Nantong, China.
authors.forename: Chongjun
authors.initials: C
authors.lastname: Zhong
authors.affiliation: Department of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital of NanTong University, Nantong, China.
authors.forename: Kun
authors.initials: K
authors.lastname: Wang
authors.affiliation: Department of Cardiology, Shanghai Putuo District Central Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Liu
authors.affiliation: School of Life Science, Shanghai University, Shanghai, China.
authors.forename: Dongchao
authors.initials: D
authors.lastname: Lv
authors.affiliation: Shanghai Institute of Biological Products Co., Ltd, Shanghai, China.
authors.forename: Bo
authors.initials: B
authors.lastname: Zheng
authors.affiliation: School of Life Science, Shanghai University, Shanghai, China.
authors.forename: Qiulian
authors.initials: Q
authors.lastname: Zhou
authors.affiliation: School of Life Science, Shanghai University, Shanghai, China.
authors.forename: Qi
authors.initials: Q
authors.lastname: Sun
authors.affiliation: School of Life Science, Shanghai University, Shanghai, China.
authors.forename: Ping
authors.initials: P
authors.lastname: Chen
authors.affiliation: Department of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital of NanTong University, Nantong, China.
authors.forename: Shengguang
authors.initials: S
authors.lastname: Ding
authors.affiliation: Department of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital of NanTong University, Nantong, China.
authors.forename: Yiming
authors.initials: Y
authors.lastname: Xu
authors.affiliation: Department of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital of NanTong University, Nantong, China.
authors.forename: Haitao
authors.initials: H
authors.lastname: Huang
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002465:Cell Movement / Q000235:genetics; D049109:Cell Proliferation; D005347:Fibroblasts / Q000166:cytology* / Q000378:metabolism*; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D009206:Myocardium / Q000166:cytology*; D051059:PTEN Phosphohydrolase / Q000235:genetics / Q000378:metabolism; D017207:Rats, Sprague-Dawley
chemical_list: C586754:MIRN19 microRNA, rat; D035683:MicroRNAs; D051059:PTEN Phosphohydrolase
keywords: Pten; cardiac fibrosis; miR-19b