Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/112924
Citations
Scopus Web of Science® Altmetric
?
?
Type: Journal article
Title: High-density lipoproteins attenuate high glucose-impaired endothelial cell signaling and functions: potential implications for improved vascular repair in diabetes
Author: Chen, X.
Duong, M.
Psaltis, P.
Bursill, C.
Nicholls, S.
Citation: Cardiovascular Diabetology, 2017; 16(1):121-1-121-9
Publisher: BioMed Central
Issue Date: 2017
ISSN: 1475-2840
1475-2840
Statement of
Responsibility: 
Xing Chen, My-Ngan Duong, Peter J. Psaltis, Christina A. Bursill and Stephen J. Nicholls
Abstract: Abnormalities of endothelial cell function are proposed to be a critical factor underlying adverse cardiovascular outcomes in the setting of hyperglycaemia. While high-density lipoproteins (HDL) have been demonstrated to be cardioprotective, the impact on the endothelium in hyperglycaemia has not been fully elucidated.Human umbilical vein endothelial cells (HUVECs) were exposed to high-glucose conditions using dextrose, the main isoform of glucose, and native HDL. HUVEC proliferation and migration were determined. The key signalling pathways that regulate endothelial cell function were also characterized.Increasing concentrations of dextrose resulted in significant reductions in HUVEC proliferation, this was attenuated by coincubation with HDL. In support of this, HDL was also found to rescue dextrose impaired expression of PCNA and the activation (phosphorylation) of the key transcription factor for proliferation ERK. Dextrose also dose-dependently inhibited HUVEC migration, which was mitigated by co-incubation with HDL. Consistent with this, HDL prevented dextrose-induced inhibition of p38 phosphorylation, responsible for cell migration. Finally, phosphorylation of the pro-survival transcription factor Akt was dose-dependently inhibited by dextrose, however, this was completely rescued by co-administration with HDL.Dextrose-induced hyperglycaemia causes the impairment of endothelial cell proliferation and migration and inhibits the activation of ERK, p38 and Akt pathways. The protective effects of HDL in this milieu highlights the potential for HDL to improve vascular repair in patients with impaired glucose homeostasis.
Keywords: HDL; hyperglycaemia; endothelial cells; atherosclerosis
Rights: © The Author(s) 2017. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
RMID: 0030076496
DOI: 10.1186/s12933-017-0605-8
Appears in Collections:Medicine publications

Files in This Item:
File Description SizeFormat 
hdl_112924.pdfPublished version1.02 MBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.