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Heart Surg Forum. 2019 Jan 28;22(1):E019-E023. doi: 10.1532/hsf.2079.

MiR-29b Inhibits Ventricular Remodeling By Activating Notch Signaling Pathway in the Rat Myocardial Infarction Model.

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Department of Child Healthcare, Linyi People's Hospital, NO. 233, Fenghuang Avenue, Jiuqu Community, Hedong District, Linyi City, 276000, Shandong Province, China.
Department of Cardiology, Jinan First People’s Hospital, NO. 132, Daming Lake Road, Lixia District, Jinan City, 250000, Shandong Province, China.
Department of Pneumology, Jinan Third People’s Hospital, NO. 1, North Street, North Industrial Road, Licheng District, Jinan City, 250101, Shandong Province, China.
Department of Cardiology, Jinan Central Hospital Affiliated to Shandong University, NO. 105, Jiefang Road, Lixia District, Jinan City, 250013, Shandong Province, China.



To study the effect of miR-29b on myocardial infarction via Notch signaling pathway in rats.


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.


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).


MiR-29b inhibited myocardial fibrosis and cardiac hypertrophy by activating the Notch signaling pathway and protected myocardium against myocardial infarction.

[Indexed for MEDLINE]

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