AI Article Synopsis

  • Coronary heart disease (CHD) is primarily caused by arteriosclerosis in coronary arteries, and this study examines the role of miR-17 in CHD.
  • Human umbilical vascular endothelial cells (HUVECs) were treated with oxidized low density lipoprotein (ox-LDL) to analyze the effects of miR-17 on cell proliferation and apoptosis using various assays.
  • The results indicate that miR-17 is upregulated in ox-LDL treated HUVECs, promotes cell survival, and may serve as a potential biomarker for CHD by regulating the expression of insulin-like Growth Factor-1 (IGF-1) and related apoptotic factors.

Article Abstract

Coronary heart disease (CHD) is one of the main risks of death, which is mainly caused by coronary arteries arteriosclerosis. The present study aims to investigate the potential roles of miR-17 in CHD. In the present study, Human umbilical vascular endothelial cells (HUVECs) were treated with oxidized low density lipoprotein (ox-LDL). qRT-PCR and western blot were used to examine the mRNA and protein levels, respectively. CCK-8 and flow cytomtry were conducted to determine the proliferation and apoptosis of ox-LDL treated HUVECs. Moreover, luciferase assay was performed to confirm whether insulin-like Growth Factor-1 (IGF-1) was a target of miR-17. The results showed that miR-17 was upregulated in ox-LDL treated HUVECs, while IGF-1 was downregulated. The luciferase activity of ox-LDL treated HUVECs was decreased after the treatment of miR-17 mimics and IGF-1 3'UTR WT. Moreover, overexpressed miR-17 promoted the cell viability and inhibited the apoptosis of ox-LDL treated HUVECs, which was more potent after the treatment of IGF-1 siRNA. Furthermore, the expression of Bax and Caspase3 was decreased, and Bcl-2 was increased in ox-LDL treated HUVECs transfected with miR-17 mimics, which was further decreased after transfection with IGF-1 siRNA. Taken together, miR-17 may regulate the proliferation and apoptosis of ox-LDL treated HUVECs. miR-17 may be a promising biomarker for CHD.

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Source
http://dx.doi.org/10.1016/j.prp.2019.152512DOI Listing

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