Association between miR-181b and PKG 1 in myocardial hypertrophy and its clinical implications

Zhong,Wei; Yang,Jun; Cao,Qian; Huan,Xiaodong

doi:10.3892/etm.2015.2647

September-2015 Volume 10 Issue 3

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September-2015 Volume 10 Issue 3

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Article Open Access

Association between miR-181b and PKG 1 in myocardial hypertrophy and its clinical implications

Authors:
- Wei Zhong
- Jun Yang
- Qian Cao
- Xiaodong Huan
View Affiliations / Copyright

Affiliations: Cadre Ward, Zaozhuang Municipal Hospital, Zaozhuang, Shandong 277101, P.R. China, Department of Cardiology, Zaozhuang Municipal Hospital, Zaozhuang, Shandong 277101, P.R. China, Department of Cardiology, Zaozhuang Hospital of Traditional Chinese Medicine, Zaozhuang, Shandong 277100, P.R. China

Copyright: © Zhong et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
Pages: 857-862
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Published online on: July 20, 2015

https://doi.org/10.3892/etm.2015.2647
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Abstract

The aim of this study was to explore the microRNA (miR)-181b expression in myocardial hypertrophy and to investigate its association with cGMP‑dependent protein kinase type I (PKG 1) in an in vitro model. The miR‑181b level in the peripheral blood was determined in patients with myocardial hypertrophy, and an in vitro model was established via phenylephrine (PE) treatment. Reverse transcription‑quantitative polymerase chain reaction analysis and western blotting were performed to detect the expression levels of miR‑181b, PKG 1 and hypertrophy-related genes. The results revealed that the expression of miR‑181b was elevated in the peripheral blood of patients with myocardial hypertrophy, and this may have contributed to the pathology and progression of the disease. When the primary myocardial cells were treated with PE, microscopic observation and flow cytometry revealed significant hypertrophy. Furthermore, upregulation of myocardial hypertrophy‑related genes, including β‑myosin heavy chain, α‑sarcomeric actinin and atrial natriuretic peptide, was observed. The miR‑181b expression level in the PE‑treated cells was elevated, while the mRNA and protein expression levels of PKG 1 were decreased, indicating a negative correlation between miR‑181b and PKG 1 in myocardial hypertrophy. In addition, when the PE‑treated primary myocardial cells were transfected with miR‑181b inhibitor, the reduced PKG 1 expression was restored and the myocardial hypertrophy alleviated, as indicated by the reduced cellular sizes and decreased expression levels of the myocardial hypertrophy‑related genes. In conclusion, miR‑181b expression has been shown to be upregulated in myocardial hypertrophy, and this may play a role in the pathogenesis of the disease by regulating the expression of PKG 1. The present findings suggest that miR‑181b is a promising molecular indicator for the clinical diagnosis and treatment of cardiac hypertrophy.

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