Premium
Aldosterone‐mediated cardiac regulation of microRNA‐21
Author(s) -
Romero Damian G.,
Price Jana E.,
Hall Michael E,
Bandyopadhyay Sibali,
Yanes Licy L.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.936.4
Subject(s) - microrna , downregulation and upregulation , aldosterone , in situ hybridization , cardiac fibrosis , biology , medicine , endocrinology , in vivo , in vitro , gene expression , microbiology and biotechnology , cancer research , heart failure , gene , biochemistry , genetics
Excess aldosterone (ALDO), along with high salt intake, causes cardiac damage. The molecular mechanisms of ALDO‐mediated cardiac injury are poorly understood. MicroRNAs (miRNAs) are endogenous, non‐coding RNAs that have important roles in cell proliferation and differentiation. We previously reported that treatment of rats with ALDO/SALT increases cardiac left ventricle miR‐21 expression and downregulation of miR‐21 exacerbated cardiac injury. We aimed to identify the cardiac cells in which miR‐21 is regulated by ALDO/SALT. Uninephrectomized male Sprague Dawley rats were treated with ALDO/SALT or vehicle for 2 weeks. Cardiomyocytes and fibroblasts were isolated and sorted using cell‐specific markers and miR‐21 expression quantified by qPCR. Cardiac fibroblasts were isolated from control rats, cultured, treated with ALDO for 24 h and miR‐21 expression quantified by qPCR. ALDO/SALT treatment increased miR‐21 expression only in the fibroblasts. In situ hybridization confirmed these results. In vitro treatment of cardiac fibroblasts with ALDO dose‐dependently increased miR‐21 expression. In summary, these results suggest that cardiac fibroblasts are a direct target of ALDO both in vitro and in vivo and modulation of cardiac fibroblast miR‐21 levels may be a novel therapeutic approach to mitigate ALDO/SALT‐mediated cardiac injury. Supported by American Heart Association Grant 12SDG8980032.