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

The role of actin depolymerizing factor in advanced glycation endproducts-induced impairment in... 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Molecular and Cellular Biochemistry Springer Journals

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

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Publisher
Springer US
Copyright
Copyright © 2017 by Springer Science+Business Media New York
Subject
Life Sciences; Biochemistry, general; Medical Biochemistry; Oncology; Cardiology
ISSN
0300-8177
eISSN
1573-4919
D.O.I.
10.1007/s11010-017-3019-8
Publisher site
See Article on Publisher Site

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