miR-17 regulates the proliferation and apoptosis of endothelial cells in coronary heart disease via targeting insulin-like-growth factor 1

• Published in: Pathology, research and practice research and practice, 2019-09, Vol.215 (9), p.152512-152512, Article 152512
• Main Authors: Chen, Zhongpu, Pan, Xiaodong, Sheng, Zulong, Yan, Gaoliang, Chen, Long, Ma, Genshan
• Format: Article
• Language: English
• Subjects: Apoptosis; Apoptosis - physiology; Cell Proliferation - physiology; Cells, Cultured; Coronary Disease - metabolism; Coronary Disease - pathology; Coronary heart disease; Human Umbilical Vein Endothelial Cells - drug effects; Human Umbilical Vein Endothelial Cells - metabolism; Human Umbilical Vein Endothelial Cells - pathology; Humans; IGF-1; Insulin-Like Growth Factor I - metabolism; Lipoproteins, LDL - toxicity; MicroRNAs - metabolism; miR-17; Proliferation
• ISSN: 0344-0338; 1618-0631
• DOI: 10.1016/j.prp.2019.152512

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.