Linc00152 suppresses apoptosis and promotes migration by sponging miR-4767 in vascular endothelial cells
Metrics: PDF 1417 views | HTML 2934 views | ?
Wei Teng1,2, Chunguang Qiu1, Zhaohui He2, Guoliang Wang2, Yongliang Xue2 and Xuezhi Hui2
1Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China
2Department of Cardiology, The First Affiliated Hospital of Henan University, Kaifeng 475000, China
Chunguang Qiu, email: [email protected]
Keywords: vascular endothelial cells, linc00152, cell apoptosis and migration, miR-4767, ceRNA
Received: February 23, 2017 Accepted: May 22, 2017 Published: June 28, 2017
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.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.