Document Type

Journal Article

Department/Unit

Department of Biology

Title

MicroRNA-15b contributes to ginsenoside-Rg1-induced angiogenesis through increased expression of VEGFR-2

Language

English

Abstract

Ginsenoside-Rg1 (Rg1) has been identified as potent proangiogenic agent, which plays an important role in wound healing promotion or treatment of ischemic injury. We previously reported that miR-214/ eNOS pathway was involved in Rg1-induced angiogenesis. Following the same microRNA microarray profiling data, we proposed miR-15b would be another microRNA candidate involved in Rg1-induced angiogenesis. Using human umbilical vein endothelial cells (HUVECs), it was showed that Rg1 could reduce miR-15b expression rapidly and steadily, leading to a temporal induction of vascular endothelial growth factor receptor-2 (VEGFR-2). The in vitro motility and tubulogenesis via VEGFR-2 in Rg1-treated HUVECs were also demonstrated. Besides, the reduction of VEGFR-2 30-UTR reporter activity by miR-15b in the luciferase reporter gene assay clearly indicated that miR-15b could affect the VEGFR-2 transcript through targeting its 30-UTR region. Diminishing expression of endogenous miR-15b could increase VEGFR-2 expression and HUVECs migration and tubulogenesis; while over-expression of miR-15b was found to associate with the reduction of VEGFR-2 expression as well as cellular migration and tubulogenesis. In vivo, artificial increment of miR-15b by injecting Pre-miR-15b precursor into zebrafish embryos was also found to significantly suppress the subintestinal vessels formation. In conclusion, our results further demonstrated the involvement of microRNAs in Rg1-induced angiogenesis. © 2013 Elsevier Inc. All rights reserved.

Keywords

Angiogenesis, Ginsenoside-Rg1, HUVECs, Microrna-15b, VEGFR-2

Publication Date

2013

Source Publication Title

Biochemical Pharmacology

Volume

86

Issue

3

Start Page

392

End Page

400

Publisher

Elsevier

DOI

10.1016/j.bcp.2013.05.006

Link to Publisher's Edition

http://dx.doi.org/10.1016/j.bcp.2013.05.006

ISSN (print)

00062952

ISSN (electronic)

18732968

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