ArticleDiabetologia2003
Oleate, not ligands of the receptor for advanced glycation end-products, promotes proliferation of human arterial smooth muscle cells.
Article in Diabetologia, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- The retinol dehydrogenase Rdh10 localizes to lipid droplets during acyl ester biosynthesis.The Journal of biological chemistry · 2013Article
- Key fatty acid combinations define vascular smooth muscle cell proliferation and viability.Lipids · 2012Article
- Distinct regulation of stearoyl-CoA desaturase 1 gene expression by cis and trans C18:1 fatty acids in human aortic smooth muscle cells.Genes & nutrition · 2012Article
- Lipid metabolic pathways as lung cancer therapeutic targets: a computational study.International journal of molecular medicine · 2012Article
- Mycophenolic acid inhibits oleic acid-induced mesangial cell activation through both cellular reactive oxygen species and inosine monophosphate dehydrogenase 2 pathways.Pediatric nephrology (Berlin, Germany) · 2009Article
- Regulation of the G2-M cell cycle progression by the ERK5-NFkappaB signaling pathway.The Journal of cell biology · 2007Article
- Article
- Fenofibrate modifies human vascular smooth muscle proteoglycans and reduces lipoprotein binding.Diabetologia · 2004Article
- Diabetes and diabetes-associated lipid abnormalities have distinct effects on initiation and progression of atherosclerotic lesions.The Journal of clinical investigation · 2004Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
aims/hypothesisDiabetes accelerates cardiovascular disease caused by atherosclerosis. Accordingly, diabetes accelerates atherosclerotic lesion progression and increases arterial smooth muscle cell proliferation. We hypothesized that diabetes can exert growth-promoting effects on smooth muscle cells via increased advanced glycation end-products or by dyslipidaemia.
methodsPrimary human arterial smooth muscle cells were stimulated with advanced glycation end-products, other ligands of the receptor for advanced glycation end-products or fatty acids common in triglycerides. Cell proliferation was measured as DNA synthesis, cell cycle distribution and cell number. Effects of oleate on cellular phospholipids, diacylglycerol, triglycerides and cholesterol esters were analyzed by thin-layer chromatography, and oleate accumulation into diacylglycerol was confirmed by gas chromatography.
resultsHuman arterial smooth muscle cells express the receptor for advanced glycation end-products, but its ligands N(epsilon)-(carboxymethyl)lysine-modified proteins, methylglyoxal-modified proteins, S100B polypeptide and amyloid-beta (1-40) peptide, exert no mitogenic action. Instead, oleate, one of the most common fatty acids in triglycerides, enhances platelet-derived growth factor-BB-mediated proliferation and oleate-containing 1,2-diacylglycerol formation in smooth muscle cells. This mitogenic effect of oleate depends on phospholipase D activity and is associated with an increased formation of oleate-enriched 1,2-diacylglycerol. CONCLUSION/
interpretationOleate, not ligands of the receptor for advanced glycation end-products, acts as an enhancer of human smooth muscle cell proliferation. Thus, lipid abnormalities, rather than hyperglycaemia, could be a major factor promoting proliferation of smooth muscle cells in atherosclerotic lesions.
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