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Publication : Inhibition of microRNA‑155 ameliorates cardiac fibrosis in the process of angiotensin II‑induced cardiac remodeling.

First Author  Wei Y Year  2017
Journal  Mol Med Rep Volume  16
Issue  5 Pages  7287-7296
PubMed ID  28944921 Mgi Jnum  J:331341
Mgi Id  MGI:6871436 Doi  10.3892/mmr.2017.7584
Citation  Wei Y, et al. (2017) Inhibition of microRNA155 ameliorates cardiac fibrosis in the process of angiotensin IIinduced cardiac remodeling. Mol Med Rep 16(5):7287-7296
abstractText  Cardiac fibrosis triggered by pressure overload represents one of the major challenges in the treatment of cardiovascular diseases. MicroRNA (miRNA/miR)155, a member of the small RNA family, has previously been demonstrated to be associated with cardiac inflammation. However, the effect of miR155 on cardiac fibrosis induced by angiotensin II (Ang II), particularly in cardiac fibroblasts, requires further investigation. The present study aimed to investigate the effect of miR155 in Ang IIinduced cardiac fibrosis using animal models and cardiac fibroblasts. Animal models were established in male miR155/ and wildtype (WT) C57Bl/6J mice (1012 weeks old) by Ang II infusion using subcutaneously implanted minipumps. After 8 weeks of Ang II infusion, the results demonstrated that the deletion of miR155 in mice markedly ameliorated ventricular remodeling compared with WT mice, as demonstrated by restricted inflammatory responses, decreased heart size, improved cardiac function and reduced myocardial fibrosis. In vitro, overexpression of miR155 in cardiac fibroblasts led to significantly increased fibroblast to myofibroblast transformation. However, this effect was abrogated by miR155 silencing. In conclusion, the results of the present study indicate that genetic loss of miR155 in mice ameliorates cardiac fibrotic remodeling following pressure overload. Therefore, inhibiting miR155 may have potential as an adjunct to reduce cardiac inflammation in the treatment of cardiac fibrosis.
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