Regulation of the atherogenic properties of vascular smooth muscle proteoglycans by oral anti hyperglycemic agents

de Dios, S, Frontanilla, K, Nigro, J, Ballinger, M, Ivey, M, Cawson, E and Little, P 2007, 'Regulation of the atherogenic properties of vascular smooth muscle proteoglycans by oral anti hyperglycemic agents', Journal of Diabetes and its Complications, vol. 21, no. 2, pp. 108-117.


Document type: Journal Article
Collection: Journal Articles

Title Regulation of the atherogenic properties of vascular smooth muscle proteoglycans by oral anti hyperglycemic agents
Author(s) de Dios, S
Frontanilla, K
Nigro, J
Ballinger, M
Ivey, M
Cawson, E
Little, P
Year 2007
Journal name Journal of Diabetes and its Complications
Volume number 21
Issue number 2
Start page 108
End page 117
Total pages 10
Publisher Elsevier Inc.
Abstract The present study aimed to investigate the actions of several classes of oral hypoglycemic agents [e.g., sulfonylureas (SUs), biguanides (BGs) and thiazolidinediones (TZDs)] in an in vitro model of lipid binding based on the "response to retention" hypothesis of atherogenesis. The incorporation of [35S]-SO4 into proteoglycans synthesized by human vascular smooth muscle cells (VSMCs) was assessed by cetylpyridinium chloride (CPC) precipitation method, proteoglycan electrophoretic mobility was evaluated by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE), and binding to low-density lipoprotein (LDL) was assessed by gel mobility shift assay (GMSA). The SUs evaluated showed no effect on [35S]-SO4 incorporation into proteoglycans. Only one BG, phenformin, caused a concentration-related inhibition of proteoglycan synthesis under basal conditions and in the presence of transforming growth factor-ß1 (TGF-ß1), caused by an inhibition of proteoglycan core protein synthesis secondary to a reduction in total protein synthesis. However, neither metformin nor phenformin (30-300 μmol/l) had any effect on the electrophoretic mobility of proteoglycans. The TZDs-troglitazone (TRO), rosiglitazone (ROS), and pioglitazone (PIO) (10, 30, and 30 μmol/l, respectively)-inhibited proteoglycan biosynthesis and stimulated total proteoglycan core protein synthesis, while TRO alone inhibited overall protein synthesis.
Keyword(s) Atherosclerosis
Oral hypoglycemic agents
Proteoglycans
Type 2 diabetes mellitus
Vascular smooth muscle cells
DOI - identifier 10.1016/j.jdiacomp.2006.03.003
Copyright notice © 2007 Elsevier Inc. All rights reserved.
ISSN 1056-8727
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