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

Abstract

// Wei Teng 1, 2 , Chunguang Qiu 1 , Zhaohui He 2 , Guoliang Wang 2 , Yongliang Xue 2 and Xuezhi Hui 2 1 Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China 2 Department of Cardiology, The First Affiliated Hospital of Henan University, Kaifeng 475000, China Correspondence to: Chunguang Qiu, email: chunguangqiuedu@163.com Keywords: vascular endothelial cells, linc00152, cell apoptosis and migration, miR-4767, ceRNA Received: February 23, 2017     Accepted: May 22, 2017     Published: June 28, 2017 ABSTRACT 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.