Arsenic-induced anti-angiogenesis via miR-425-5p-regulated CCM3

Gao, Y; Yin, Y; Xing, X; Zhao, Z; Lu, Y; Sun, Y; Zhuang, Z; Wang, M; Ji, W; He, Y

HERO ID

3379064

Reference Type

Journal Article

Year

2016

Language

English

PMID

27132035

HERO ID 3379064
In Press No
Year 2016
Title Arsenic-induced anti-angiogenesis via miR-425-5p-regulated CCM3
Authors Gao, Y; Yin, Y; Xing, X; Zhao, Z; Lu, Y; Sun, Y; Zhuang, Z; Wang, M; Ji, W; He, Y
Journal Toxicology Letters
Volume 254
Page Numbers 22-31
Abstract Human exposure to drinking water contaminated with arsenic is a serious global health concern and it predisposes people to cardiovascular diseases, such as hypertension, atherosclerosis, and microvascular diseases. Although accumulating evidence supports a role for angiogenesis responses to arsenic in the pathogenesis of the cardiovascular disease, the detailed molecular mechanism is not well understood. We aimed to determine the role and mechanism of microRNA (miRNA) in arsenic-induced angiogenesis. In our present study, sodium arsenite (NaAsO2) inhibited angiogenesis by decreasing cells proliferation, migration and tube formation in HUVECs. After NaAsO2 treatment, we found the expression of microRNA-425-5p (miR-425-5p) was reduced in vitro and in vivo and over-expression of miR-425-5p reversed the NaAsO2-induced anti-angiogenesis through its direct target cerebral cavernous malformation 3 (CCM3). Furthermore, we showed that NaAsO2 up-regulated CCM3 expression in vitro and in vivo. In addition, we demonstrated that inhibition of Notch and activation of VEGF/p38 signaling were involved in miR-425-5p blocking NaAsO2-induced anti-angiogenesis.
Doi 10.1016/j.toxlet.2016.04.023
Pmid 27132035
Wosid WOS:000376190300003
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English
Keyword Angiogenesis; Arsenic; MicroRNA-425-5p; Signaling pathway