OBJECTIVE: MiR-155-5p has various biological cellular functions in diverse pathology, including cardiovascular disease. Nevertheless, the role of miR-155-5p in atherosclerosis is still not well known.
PATIENTS AND METHODS: The levels of miR-155-5p and AKT Serine/Threonine Kinase 1 (AKT1) in plasma samples from patients with atherosclerotic CAD were detected using quantitative Real-time PCR (qRT-PCR). Cell counting kit-8 (CCK-8) assay was used to analyze the proliferation of vascular smooth muscle cells (VSMCs) and human umbilical vein endothelial cells (HUVECs) in vitro. The migration of VSMCs and HUVECs was detected using wound healing assay. The invasion of VSMCs and HUVECs using was determined using the transwell invasion assay. The expression of AKT1 was measured using immunofluorescence staining analysis.
RESULTS: MiR-155-5p was down-regulated in patients with atherosclerotic CAD. Up-regulation of miR-155-5p inhibited the proliferation, migration and invasion of VSMCs and HUVECs. Bioinformatics analysis and luciferase reporter assay indicated that AKT1 was the direct target of miR-155-5p and miR-155-5p bound to the 3’-untranslated region (3’-UTR) of AKT1. The expression of AKT1 was reduced in cell that was transfected with miR-155-5p. Up-regulation of AKT1 rescued the suppressive effect of miR-155-5p on the growth, migration and invasion of VSMCs and HUVECs. Down-expression of AKT1 partially neutralized the impacts of miR-155-5p on the growth, invasion and migration of VSMCs and HUVECs. Finally, we found that AKT1 was over-regulated in plasma samples of patients with atherosclerotic CAD and its level was negative with the level of miR-155-5p.
CONCLUSIONS: Our study demonstrates that miR-155-5p suppresses the proliferation, migration and invasion of VSMCs and HUVECs through regulating AKT1, which provides the new insights into the precise role of miR-155-5p in atherosclerosis.Free PDF Download
To cite this article
L. Chen, S.-Y. Zheng, C.-Q. Yang, B.-M. Ma, D. Jiang
MiR-155-5p inhibits the proliferation and migration of VSMCs and HUVECs in atherosclerosis by targeting AKT1
Eur Rev Med Pharmacol Sci
Vol. 23 - N. 5