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1.
Genet Mol Res ; 15(2)2016 Jun 24.
Article de Anglais | MEDLINE | ID: mdl-27420956

RÉSUMÉ

Published online: December 28, 2015 (DOI: 10.4238/2015.December.28.19). Corrected after publication: June 24, 2016 (DOI: 10.4238/gmr.150267961). There is a change in the corresponding author, who should be Y.F. Liu.

2.
Genet Mol Res ; 14(4): 18703-12, 2015 Dec 29.
Article de Anglais | MEDLINE | ID: mdl-26782520

RÉSUMÉ

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. Inhibition of the NF- κB pathway significantly decreased the rate of vascular smooth muscle cell apoptosis in coronary heart disease rats (P = 0.0038). In conclusion, miRNA- 146a was found to induce vascular smooth muscle cell apoptosis in rats with coronary heart disease via the activation of the NF-κB signal pathway.


Sujet(s)
Apoptose/génétique , Maladie des artères coronaires/génétique , Maladie des artères coronaires/métabolisme , microARN/génétique , Myocytes du muscle lisse/métabolisme , Facteur de transcription NF-kappa B/métabolisme , Transduction du signal , Animaux , Caspase-3/métabolisme , Modèles animaux de maladie humaine , Expression des gènes , Mâle , Rats
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