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miR-98 inhibits cell proliferation and induces cell apoptosis by targeting MAPK6 in HUVECs
The aim of current study was to explore the role of microRNA (miR)-98 in atherosclerosis. Human vascular endothelial cells (HVECs) were isolated from the peripheral blood of healthy volunteers and patients with atherosclerosis. Compared with endothelial cells from the healthy control group, the expr...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5795499/ https://www.ncbi.nlm.nih.gov/pubmed/29456679 http://dx.doi.org/10.3892/etm.2018.5735 |
Sumario: | The aim of current study was to explore the role of microRNA (miR)-98 in atherosclerosis. Human vascular endothelial cells (HVECs) were isolated from the peripheral blood of healthy volunteers and patients with atherosclerosis. Compared with endothelial cells from the healthy control group, the expression level of mitogen activated protein kinase (MAPK)6 was significantly upregulated and miR-98 was downregulated in the endothelial cells of patients with atherosclerosis. The human umbilical vein endothelial cell line (HUVEC) was adopted to perform in vitro studies. Overexpression of miR-98 reduced the proliferation and induced the apoptosis of HUVECs, which were revealed using an MTT assay, and flow cytometry assay, respectively. The aforementioned influences of miR-98 on HUVECs were mediated by targeting MAPK6, which was verified using luciferase assays. Additionally, the overexpression of miR-98 reduced the protein level of apoptosis regulator Bcl-2 and MAPK6; however, it induced the protein expression of caspase-3 and apoptosis regulator Bax. In conclusion, these findings demonstrate that miR-98 is an important regulator of atherosclerosis, suggesting that miR-98 may be a potential therapeutic target for the treatment of atherosclerosis. |
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