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2017 ; 16
(5
): 7287-7296
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Inhibition of microRNA?155 ameliorates cardiac fibrosis in the process of
angiotensin II?induced cardiac remodeling
#MMPMID28944921
Wei Y
; Yan X
; Yan L
; Hu F
; Ma W
; Wang Y
; Lu S
; Zeng Q
; Wang Z
Mol Med Rep
2017[Nov]; 16
(5
): 7287-7296
PMID28944921
show ga
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 miR?155 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 miR?155 in Ang II?induced cardiac fibrosis using animal models and cardiac
fibroblasts. Animal models were established in male miR?155?/? and wild?type (WT)
C57Bl/6J mice (10?12 weeks old) by Ang II infusion using subcutaneously implanted
minipumps. After 8 weeks of Ang II infusion, the results demonstrated that the
deletion of miR?155 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 miR?155 in cardiac fibroblasts led to significantly increased
fibroblast to myofibroblast transformation. However, this effect was abrogated by
miR?155 silencing. In conclusion, the results of the present study indicate that
genetic loss of miR?155 in mice ameliorates cardiac fibrotic remodeling following
pressure overload. Therefore, inhibiting miR?155 may have potential as an adjunct
to reduce cardiac inflammation in the treatment of cardiac fibrosis.