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

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 profili...

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Bibliographic Details
Published in:Biochemical pharmacology 2013-08, Vol.86 (3), p.392-400
Main Authors: Chan, L.S., Yue, Patrick Y.K., Wong, Y.Y., Wong, Ricky N.S.
Format: Article
Language:English
Subjects:
Angiogenesis
Angiogenesis Inducing Agents - pharmacology
Animals
Cell Movement - drug effects
Cell Movement - physiology
Cells, Cultured
Ginsenoside-Rg1
Ginsenosides - physiology
Human Umbilical Vein Endothelial Cells
Humans
HUVECs
Microrna-15b
MicroRNAs - physiology
Up-Regulation - physiology
Vascular Endothelial Growth Factor Receptor-2 - biosynthesis
VEGFR-2
Zebrafish
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Summary: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 3′-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 3′-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.
ISSN:0006-2952
1873-2968
DOI:10.1016/j.bcp.2013.05.006