AMP-Activated Protein Kinase Attenuates High Salt-Induced Activation of Epithelial Sodium Channels (ENaC) in Human Umbilical Vein Endothelial Cells
Joint Authors
Wang, Qiushi
Song, Binlin
Li, Xinyuan
Zhang, Zhi-Ren
Ma, He-Ping
Zheng, Wei-Wan
Liu, Hui-Bin
Wang, Zi-Rui
Hu, Qing-Qing
Li, Yu-Xia
Lou, Jie
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2016, Issue 2016 (31 Dec. 2016), pp.1-11, 11 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2016-08-22
Country of Publication
Egypt
No. of Pages
11
Main Subjects
Abstract EN
Recent studies suggest that the epithelial sodium channel (ENaC) is expressed in the endothelial cells.
To test whether high salt affects the NO production via regulation of endothelial ENaC, human umbilical vein endothelial cells (HUVECs) were incubated in solutions containing either normal or high sodium (additional 20 mM NaCl).
Our data showed that high sodium treatment significantly increased α-, β-, and γ-ENaC expression levels in HUVECs.
Using the cell-attached patch-clamp technique, we demonstrated that high sodium treatment significantly increased ENaC open probability ( P O ).
Moreover, nitric oxide synthase (eNOS) phosphorylation (Ser 1177) levels and NO production were significantly decreased by high sodium in HUVECs; the effects of high sodium on eNOS phosphorylation and NO production were inhibited by a specific ENaC blocker, amiloride.
Our results showed that high sodium decreased AMP-activated kinase (AMPK) phosphorylation in endothelial cells.
On the other hand, metformin, an AMPK activator, prevented high sodium-induced upregulation of ENaC expression and P O .
Moreover, metformin prevented high salt-induced decrease in NO production and eNOS phosphorylation.
These results suggest that high sodium stimulates ENaC activation by negatively modulating AMPK activity, thereby leading to reduction in eNOS activity and NO production in endothelial cells.
American Psychological Association (APA)
Zheng, Wei-Wan& Li, Xinyuan& Liu, Hui-Bin& Wang, Zi-Rui& Hu, Qing-Qing& Li, Yu-Xia…[et al.]. 2016. AMP-Activated Protein Kinase Attenuates High Salt-Induced Activation of Epithelial Sodium Channels (ENaC) in Human Umbilical Vein Endothelial Cells. Oxidative Medicine and Cellular Longevity،Vol. 2016, no. 2016, pp.1-11.
https://search.emarefa.net/detail/BIM-1113622
Modern Language Association (MLA)
Zheng, Wei-Wan…[et al.]. AMP-Activated Protein Kinase Attenuates High Salt-Induced Activation of Epithelial Sodium Channels (ENaC) in Human Umbilical Vein Endothelial Cells. Oxidative Medicine and Cellular Longevity No. 2016 (2016), pp.1-11.
https://search.emarefa.net/detail/BIM-1113622
American Medical Association (AMA)
Zheng, Wei-Wan& Li, Xinyuan& Liu, Hui-Bin& Wang, Zi-Rui& Hu, Qing-Qing& Li, Yu-Xia…[et al.]. AMP-Activated Protein Kinase Attenuates High Salt-Induced Activation of Epithelial Sodium Channels (ENaC) in Human Umbilical Vein Endothelial Cells. Oxidative Medicine and Cellular Longevity. 2016. Vol. 2016, no. 2016, pp.1-11.
https://search.emarefa.net/detail/BIM-1113622
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1113622