Open AccessMiR-29b Inhibits Ventricular Remodeling By Activating Notch Signaling Pathway in the Rat Myocardial Infarction Model
Author(s) -
Yang Liu,
Hongliang Wang,
Xiudan Wang,
Guohong Xie
Publication year - 2019
Publication title -
the heart surgery forum/the heart surgery forum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.255
H-Index - 38
eISSN - 1522-6662
pISSN - 1098-3511
DOI - 10.1532/hsf.2079
Subject(s) - medicine , myocardial infarction , rat model , infarction , ventricular remodeling , downregulation and upregulation , notch signaling pathway , fibrosis , blot , western blot , endocrinology , signal transduction , transfection , cardiology , receptor , microbiology and biotechnology , biochemistry , biology , gene
Background: To study the effect of miR-29b on myocardial infarction via Notch signaling pathway in rats.
Methods: The rat acute myocardial infarction (AMI) models were established and were divided into AMI group, sham group and normal group (N = 10 in each group). HE (Hemotoxylin and eosin) staining was used to detect whether the model was constructed successfully. MiR-29b mimics, inhibitors, mimics negative control (NC) were transfected into H9c2 (2-1) cells. Then, cells were divided into a mimics group, inhibitor group, NC group, and blank group. The relative expression levels of miR-29b, Notch1, DII4 and Hesl were detected by qRT-PCR. The expression of NICD1 was detected by Western blotting.
Results: The rat AMI model was successfully constructed. Compared with normal and sham groups, the miR-29b expression was down-regulated, while the expression of Notch1, DII4 and Hesl was increased, and the NICD1 protein expression was increased in the myocardial infarction area of the AMI group (P < .05). Compared with the NC and blank groups, the relative expression of Notch1, DII4, Hesl and NICD1 were upregulated in the mimics group (P < .05), whereas the expression of Notch1, DII4, Hesl and NICD1 in the inhibitor group was decreased (P < .05).
Conclusion: MiR-29b inhibited myocardial fibrosis and cardiac hypertrophy by activating the Notch signaling pathway and protected myocardium against myocardial infarction.