Qiang Fu1, Tao-Ran Mo2, Xiao-Yang Hu1, Yin Fu1, Ji Li3. 1. Department of Chinese Formulae, Heilongjiang University of Chinese Medicine, No. 24, Heping Road, Xiangfang District, Harbin, 150040, Heilongjiang, China. 2. Department of Nephrology, The First Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine, Harbin, 150040, Heilongjiang, China. 3. Department of Chinese Formulae, Heilongjiang University of Chinese Medicine, No. 24, Heping Road, Xiangfang District, Harbin, 150040, Heilongjiang, China. motaoran@163.com.
Abstract
OBJECTIVE: Myocardial infarction (MI) is a prevalent cardiovascular puzzle and a mainspring of disease-induced mortality. We performed this investigation to detect the role of putative important miRNAs or genes in MI. RESULTS: CCL20 may be a potential therapeutic target, which was directly targeted and negatively regulated by miR-19a. CCL20 expression was significantly increased in MI tissue samples, but miR-19a was expressed at lower levels in MI. H/R treatment inhibited cell viability and induced an increase of apoptotic rate compared with Sham group. However, miR-19a mimic relieved the H/R-stimulated injury to cardiomyocytes. Protective effect of miR-19a against H/R in cardiomyocytes was reversed by CCL20 enhancement, and MAPK pathway was inactivated during this progression. CONCLUSIONS: miR-19a eliminates the H/R-induced injury in cardiomyocytes through directly targeting CCL20 and attenuating the activity of MAPK signaling pathway. These observations highlighted the therapeutic roles of miR-19a and CCL20 for MI treatment.
OBJECTIVE:Myocardial infarction (MI) is a prevalent cardiovascular puzzle and a mainspring of disease-induced mortality. We performed this investigation to detect the role of putative important miRNAs or genes in MI. RESULTS:CCL20 may be a potential therapeutic target, which was directly targeted and negatively regulated by miR-19a. CCL20 expression was significantly increased in MI tissue samples, but miR-19a was expressed at lower levels in MI. H/R treatment inhibited cell viability and induced an increase of apoptotic rate compared with Sham group. However, miR-19a mimic relieved the H/R-stimulated injury to cardiomyocytes. Protective effect of miR-19a against H/R in cardiomyocytes was reversed by CCL20 enhancement, and MAPK pathway was inactivated during this progression. CONCLUSIONS:miR-19a eliminates the H/R-induced injury in cardiomyocytes through directly targeting CCL20 and attenuating the activity of MAPK signaling pathway. These observations highlighted the therapeutic roles of miR-19a and CCL20 for MI treatment.
Authors: Nada Alaaeddine; John Antoniou; Mayssam Moussa; George Hilal; Gaby Kreichaty; Ismat Ghanem; Wissam Abouchedid; Elie Saghbini; John A Di Battista Journal: Inflamm Res Date: 2015-07-20 Impact factor: 4.575