miRNA-146a induces vascular smooth muscle cell apoptosis in a rat model of coronary heart disease via NF-κB pathway

Genetics and Molecular Research : GMR
Z W WuB Li

Abstract

The aim of this study was to investigate the role of miRNA-146a in modulating the function of vascular smooth muscle cells in a rat model of coronary heart disease. Vascular smooth muscle cells were isolated and cultured from the rat coronary heart disease model and normal rats (controls). miRNA-146a levels were measured in vascular smooth muscle cells obtained from rats with coronary heart disease and control rats. The proliferation, growth, apoptosis, and activation of the NF-κB pathway in the vascular smooth muscle cells were detected using the MTT assay and flow cytometry, respectively. The role of the NF-κB pathway in modulating the apoptosis of vascular smooth muscle cells was investigated by measuring the reactivity of the cells to an NF-κB pathway inhibitor (TPCA-1). Vascular smooth muscle cells from the disease model exhibited higher levels of miRNA-146a than that by the normal controls (P = 0.0024). The vascular smooth muscle cells obtained from rats with coronary heart disease showed decreased proliferation and growth and increased apoptosis. miRNA-146a overexpression elevated the rate of cell apoptosis. The NF-κB pathway was activated in vascular smooth muscle cells obtained from rats with coronary heart disease. In...Continue Reading

Citations

Feb 14, 2020·Journal of Cellular Physiology·Che WangQingman Li
Mar 15, 2019·Experimental and Therapeutic Medicine·Xiao-Lin MaRui Fan
Mar 25, 2019·Experimental and Therapeutic Medicine·Xinjing ChenZhiliang Li
Jul 10, 2019·Experimental and Therapeutic Medicine·Jin XieWenxing Fan
Jan 18, 2017·BioMed Research International·Xiao LinYou-Shuo Liu
Dec 23, 2021·Experimental and Therapeutic Medicine·Dong Wang, Caiyun Yan

❮ Previous
Next ❯

Related Concepts

Related Feeds

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis