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miR-487b promotes human umbilical vein endothelial cell proliferation, migration, invasion and tube formation through regulating THBS1.
- Source :
-
Neuroscience letters [Neurosci Lett] 2015 Mar 30; Vol. 591, pp. 1-7. Date of Electronic Publication: 2015 Feb 04. - Publication Year :
- 2015
-
Abstract
- Angiogenesis is essential for recovery from various neurovascular diseases, such as ischemic stroke. Previous studies have revealed the regulatory role of MicroRNAs in angiogenesis in various types of cancer cells. However, the role of miR-487b in angiogenesis and how it regulates the angiogenic process of endothelial cells remain unclear. In this study, we found miR-487b was up-regulated in the plasma of ischemic stroke patients. Further, over-expression of miR-487b enhanced cell proliferation, migration, invasion and tube formation in human umbilical vein endothelial cells. Using bioinformatic analysis, we found a putative binding site of miR-487b in the 3' untranslated regions of Thrombospondin 1 mRNA, an endogenous inhibitor of angiogenesis. This direct binding was confirmed by luciferase assay. These results demonstrate that miR-487b regulates angiogenesis by directly targeting THBS1 in HUVECs, indicating that miR-487b may contribute to angiogenesis and the functional recovery from ischemic stroke. miR-487b could represent a potential therapeutic option for neurovascular disease.<br /> (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)
- Subjects :
- 3' Untranslated Regions
Adult
Aged
Brain Ischemia metabolism
Brain Ischemia pathology
Cell Movement
Cell Proliferation
Female
Human Umbilical Vein Endothelial Cells cytology
Humans
Male
MicroRNAs genetics
Middle Aged
Stroke etiology
Stroke metabolism
Stroke pathology
Thrombospondin 1 genetics
Up-Regulation
Human Umbilical Vein Endothelial Cells physiology
MicroRNAs metabolism
Neovascularization, Physiologic
Thrombospondin 1 metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1872-7972
- Volume :
- 591
- Database :
- MEDLINE
- Journal :
- Neuroscience letters
- Publication Type :
- Academic Journal
- Accession number :
- 25660232
- Full Text :
- https://doi.org/10.1016/j.neulet.2015.02.002