Linc00152 suppresses apoptosis and promotes migration by sponging miR-4767 in vascular endothelial cells.

PMID 29156700


Dysfunction of vascular endothelial cells (VECs), such as increased apoptosis and diminished migration, is closely connected with most cardiovascular diseases and angiogenesis-related events. LncRNAs have been involved in regulation of many pathological processes, but their roles in vascular endothelial function are hardly underreported. Here, we explore the role of a intergenic lncRNA named linc00152 in the apoptosis and migration of VECs. We found that linc00152 was downregulated in human umbilical vein VECs (HUVECs) in a dose- and time-dependent manner following treatment with oxLDL, which is a typical proinflammatory factor in the initiation and progression of vascular endothelial dysfunction. Gain- and loss-function experiments indicated that linc00152 distinctly inhibited apoptosis and improved migration in oxLDL-treated HUVECs. By sponging miR-4767, linc00152 positively regulated the expression of Bcl2L12 and EGFR proteins. Moreover, blocking miR-4767 rescued the decrease of Bcl2L12 and EGFR caused by linc00152 knockdown, as well as the changes in cell apoptosis and migration. Our findings propose a novel role of linc00152 in the improvement of vascular endothelial function and a potential target for the therapy of some cardiovascular diseases.

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