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The role of actin depolymerizing factor in advanced glycation endproducts-induced impairment in mouse brain microvascular endothelial cells.

Abstract：

:Endothelial dysfunction is one of the most important pathological events during the development of several diabetic complications including stroke. The aim of this work was to investigate the role of actin depolymerizing factor (ADF) in advanced glycation endproducts (AGEs)-induced impairment in mouse brain microvascular endothelial cells (MBMECs). Incubation of MBMECs with AGEs led to downregulation of expression of ADF, which was reversed by treatment with soluble receptor of AGEs or tempol (an antioxidant). Incubation of MBMECs with AGEs enhanced ratio of F/G-actin, increased endothelial permeability and reduced vasculogenic property, which was attenuated by overexpression of ADF. Furthermore, overexpression of ADF attenuated AGEs-induced downregulation of zonula occludens-1 and dephosphorylation of vascular endothelial growth factor receptor 2. Incubation of MBMECs with AGEs downregulated dimethylarginine dimethylaminohydrolase 2, enhanced formation of asymmetric dimethylarginine and reduced formation of nitric oxide, which was attenuated by overexpression of ADF. Incubation of MBMECs with AGEs induced activation of NF-κB, upregulated RAGE and enhanced formation of reactive oxygen species, which was attenuated by overexpression of ADF. Additionally, knockdown of ADF aggravated AGEs-induced impairment in endothelial permeability and vasculogenic property in MBMECs. In conclusion, AGEs treatment increased endothelial permeability and reduced vasculogenic property of MBMECs, at least in part, via downregulation of ADF.

journal_name

Mol Cell Biochem

journal_title

Molecular and cellular biochemistry

authors

Liu X,Zhang R,Di H,Zhao D,Wang J

doi

10.1007/s11010-017-3019-8

subject

Has Abstract

pub_date

2017-09-01 00:00:00

pages

103-112

issue

1-2

eissn

0300-8177

issn

1573-4919

pii

10.1007/s11010-017-3019-8

journal_volume

433

pub_type

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