Molecular mechanisms in microRNA-mediated TRB3 gene and hypertension left ventricular hypertrophy

Zeng,Jun-Yi; Lei,Juan; Wei,Yun-Feng; Zheng,Ze-Qi; Zhang,Wan; Fu,Yong-Nan; Wen,Tong; Yi,Da-Song; Ding,Lu

doi:10.3892/etm.2017.4220

Molecular mechanisms in microRNA-mediated TRB3 gene and hypertension left ventricular hypertrophy

Authors:
- Jun-Yi Zeng
- Juan Lei
- Yun-Feng Wei
- Ze-Qi Zheng
- Wan Zhang
- Yong-Nan Fu
- Tong Wen
- Da-Song Yi
- Lu Ding
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Affiliations: Department of Cardiology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China, Jiangxi Modern Polytechnic College, Nanchang, Jiangxi 330095, P.R. China, Jiangxi Institute of Hypertension, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China
Published online on: March 10, 2017 https://doi.org/10.3892/etm.2017.4220
Pages: 1907-1911
Copyright: © Zeng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The present study investigated the relationship between microRNA-mediated TRB3 gene and hypertension left ventricular hypertrophy at the molecular level. Polymorphic site in TRB3 gene was identified by direct PCR method, and the correlation between the SNP site and ventricular hypertrophy was determined. MicroRNAs target gene sequence interacting on the TRB3 polymorphic site was screened by bioinformatics, and the effect of microRNAs on the TRB3 polymorphic site was finally verified by luciferase test. Two polymorphic sites rs6186912 and rs6186923 were found in the TRB3 gene, and the direct relationship between rs6186923 polymorphic site and the hypertension left ventricular hypertrophy in patients with myocardial hypertrophy was compared and analyzed. Pictar software was used to analyze the effect of miR-100 on rs6186923, and the argumentation was verified by luciferase test. In conclusion, the study showed that the TRB3 gene polymorphism rs6186923 was able to affect the TRB3 gene by affecting the binding of miR-100, which indirectly caused the formation of hypertension left ventricular hypertrophy.

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