In:
Cardiovascular Therapeutics, Wiley, Vol. 33, No. 3 ( 2015-06), p. 109-117
Abstract:
To investigate the cardioprotective effect of Micro RNA ‐21 (miR‐21) in murine myocardial infarction ( MI ). Methods Forty C57 BL /6 male mice were divided into sham group, MI group, LV ‐ GFP group, and miR‐21 group. Mice in the MI group, LV ‐ GFP group, and miR‐21 group were subjected to MI by left anterior descending artery ( LAD ) ligation, while chest was opened/closed without ligation in sham group. In MI group, expression of miR‐21 in the MI area and its surrounding areas was detected at 1st, 2nd, and 4th week after experiment. Subsequently, lentivirus expressing miR‐21 and lentivirus that did not express miR‐21 were transfected into mice left ventricular cavity of miR‐21 group and LV ‐ GFP group, respectively. Cardiac function, MI size, miR‐21 expression, collagen I level, fibronectin content, number of α ‐ SMA ‐positive cells, number of apoptotic cells, apoptosis‐related factors were compared between the three groups. Results Compared with sham group, miR‐21 levels in MI group were significantly decreased in the 1st week and 2nd week, but were almost the same in the 4th week. Left ventricular fractional shortening ( LVFS ) and left ventricular ejection fraction ( LVEF ) in the miR‐21 group improved compared to the LV ‐ GFP group. In miR‐21 group, myocardial infarct size reduced by 36.9% in comparison with LV ‐ GFP group. Compared to sham group, miR‐21 expression in the miR‐21 group and LV ‐ GFP group decreased significantly. In the miR‐21 group, collagen I level, fibronectin content and number of α ‐ SMA ‐positive cells of miR‐21 decreased significantly compared to the LV ‐ GFP group. The number of apoptotic cells in the MI areas of the miR‐21 group was significantly less than the LV ‐ GFP group. Compared with the LV ‐ GFP group, Bcl‐2 level and the ratio of Bcl‐2 to Bax were significantly increased, and the levels of Bax and Caspase‐3 decreased. Conclusions Our results suggest miR‐21 is an important regulatory molecule in the pathophysiology of MI .
Type of Medium:
Online Resource
ISSN:
1755-5914
,
1755-5922
DOI:
10.1111/cdr.2015.33.issue-3
DOI:
10.1111/1755-5922.12118
Language:
English
Publisher:
Wiley
Publication Date:
2015
detail.hit.zdb_id:
2417088-4
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