Oleate, not ligands of the receptor for advanced glycation end-products, promotes proliferation of human arterial smooth muscle cells

Renard, Claire-Angélique; Askari, Bardia; Suzuki, Lucy A.; Kramer, Farah; Bornfeldt, Karin E.

doi:10.1007/s00125-003-1247-9

Cited by 21 publications

(21 citation statements)

References 65 publications

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“…Very recently, it has been shown that RAGE activation is involved in the activation of the TGF--ROCK1 pathway in mouse aortic VSMC 22) . In contrast, several previous studies have shown that cultured VSMC barely expressing RAGE were unable to respond to RAGE ligands 5,23) . We also failed to detect RAGE expression and responses to S100B in our parent A10 cells and primary cultured rat VSMCs (unpublished observation).…”

Section: Discussioncontrasting

confidence: 59%

Overexpression of Receptor for Advanced Glycation End Products Induces Monocyte Chemoattractant Protein-1 Expression in Rat Vascular Smooth Muscle Cell Line

Hayakawa

Yoshimoto

Sekizawa

et al. 2012

JAT

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Aim:The receptor for advanced glycation end-products (RAGE) has been suggested to play a pivotal role in the development of diabetic vasculopathy and atherosclerosis; however, due to its low expression, the physiological role of RAGE in vascular smooth muscle cells (VSMC) remains unknown. Methods: Using VSMC lines stably expressing RAGE (RAGE-A10), we studied the molecular mechanism by which S100B, a RAGE ligand, induces proinflammatory gene expression. Results: S100B induced NF-B activation and the expression of several proinflammatory genes (MCP-1, IL-6, ICAM-1) at mRNA and protein levels in RAGE-A10, among which MCP-1 expression was the most robust. S100B-induced MCP-1 expression was dose-dependently blocked by inhibitors of JNK (SP600125), p38 (SB203580), MEK-1 (U0126) as well as NF-B (Bay117085). In RAGE-A10, S100B activated JNK, MEK-1 and p38. S100B-induced MCP-1 promoter activity via NF-B binding sites and nuclear translocation of NF-B p65 subunit were blocked by SP600125, U0126, and SB203580 in RAGE-A10. Conclusion: Our study demonstrates that S100B increased MCP-1 expression via NF-B and mitogen-activated protein kinase (JNK, ERK1/2, and p38) pathways in RAGE-overexpressed A10 cell lines. Thus, RAGE-A10 could be a useful cell model for studying the molecular mechanism(s) of upregulated RAGE in the vasculature. J Atheroscler Thromb, 2012; 19:13-22.

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Section: Discussioncontrasting

confidence: 59%

Overexpression of Receptor for Advanced Glycation End Products Induces Monocyte Chemoattractant Protein-1 Expression in Rat Vascular Smooth Muscle Cell Line

Hayakawa

Yoshimoto

Sekizawa

et al. 2012

JAT

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“…1c). In contrast, oleic acid is able to enhance proliferation of HASMC induced by promitogenic factors (data not shown and Renard et al 2003). Scd1 expression is associated with the regulation of survival and proliferation signals in normal and cancer cells.…”

Section: Discussionmentioning

confidence: 88%

Distinct regulation of stearoyl-CoA desaturase 1 gene expression by cis and trans C18:1 fatty acids in human aortic smooth muscle cells

et al. 2011

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Consumption of trans fatty acids is positively correlated with cardiovascular diseases and with atherogenic risk factors. Trans fatty acids might play their atherogenic effects through lipid metabolism alteration of vascular cells. Accumulation of lipids in vascular smooth muscle cells is a feature of atherosclerosis and a consequence of lipid metabolism alteration. Stearoyl-CoA desaturase 1 (scd1) catalyses the production of monounsaturated fatty acids (e.g. oleic acid) and its expression is associated with lipogenesis induction and with atherosclerosis development. We were interested in analysing the regulation of delta-9 desaturation rate and scd1 expression in human aortic smooth muscle cells (HASMC) exposed to cis and trans C18:1 fatty acid isomers (cis-9 oleic acid, trans-11 vaccenic acid or trans-9 elaidic acid) for 48 h at 100 lM. Treatment of HASMC with these C18:1 fatty acid isomers led to differential effects on delta-9 desaturation; oleic acid repressed the desaturation rate more potently than trans-11 vaccenic acid, whereas trans-9 elaidic acid increased the delta-9 desaturation rate. We then correlated the delta-9 desaturation rate with the expression of scd1 protein and mRNA. We showed that C18:1 fatty acids controlled the expression of scd1 at the transcriptional level in HASMC, leading to an increase in scd1 mRNA content by trans-9 elaidic acid treatment, whereas a decrease in scd1 mRNA content was observed with cis-9 oleic acid and trans-11 vaccenic acid treatments. Altogether, this work highlights a differential capability of C18:1 fatty acid isomers to control scd1 gene expression, which presumes of different consequent effects on cell functions.

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“…We included insulin with PDGF; however, it would also be interesting to stimulate VSMCs with agents that correlate with other metabolic abnormalities of diabetes, such as fatty acids [9,31].…”

Section: Discussionmentioning

confidence: 99%

Fenofibrate modifies human vascular smooth muscle proteoglycans and reduces lipoprotein binding

et al. 2004

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Aims/hypothesis. Vascular disease in type 2 diabetes is associated with an up-regulation of atherogenic growth factors, which stimulate matrix synthesis including proteoglycans. We have examined the direct actions of fenofibrate on human vascular smooth muscle cells (VSMCs) and have specifically investigated proteoglycan synthesis and binding to LDL. Methods. Proteoglycans synthesised by human VSMCs treated with fenofibrate (30 µmol/l) were assessed for binding to human LDL using a gel mobility shift assay, metabolically labelled with [ 35 S]-sulphate and quantitated by cetylpyridinium chloride. They were then assessed for electrophoretic mobility by SDS-PAGE, for size by gel filtration, for sulphation pattern by fluorophore-assisted carbohydrate electrophoresis, and for glycosaminoglycan (GAG) composition by enzyme digestion. Results. Proteoglycans synthesised in the presence of fenofibrate showed an increase in the half-maximum saturation concentration of LDL from 36.8±12.4 µg/ml to 77.7±17 µg/ml under basal conditions, from 24.9±4.6 µg/ml to 39.1±6.1 µg/ml in the presence of TGF-β1, and from 9.5±4.4 µg/ml to 31.1±3.4 µg/ml in the presence of platelet-derived growth factor/insulin. Fenofibrate treatment in the presence of TGF-β1 inhibited the incorporation of [ 35 S]-sulphate into secreted and cell-associated proteoglycans synthesised by human VSMCs by 59.2% (p<0.01) and 39.8% (p<0.01) respectively. The changes in sulphate incorporation following treatment with fenofibrate were associated with a concentration-related increase in the electrophoretic mobility due to a reduction in GAG length. There was no change in the sulphation pattern; however, there was an alteration in the disaccharide composition of the GAGs. Conclusions/interpretation. Fenofibrate modifies the structure of vascular proteoglycans by reducing the length of the GAG chains and GAG composition, resulting in reduced binding to human LDL, a mechanism which may lead to a reduction of atherosclerosis and cardiovascular disease in people with diabetes treated with fenofibrate.

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Oleate, not ligands of the receptor for advanced glycation end-products, promotes proliferation of human arterial smooth muscle cells

Cited by 21 publications

References 65 publications

Overexpression of Receptor for Advanced Glycation End Products Induces Monocyte Chemoattractant Protein-1 Expression in Rat Vascular Smooth Muscle Cell Line

Overexpression of Receptor for Advanced Glycation End Products Induces Monocyte Chemoattractant Protein-1 Expression in Rat Vascular Smooth Muscle Cell Line

Distinct regulation of stearoyl-CoA desaturase 1 gene expression by cis and trans C18:1 fatty acids in human aortic smooth muscle cells

Fenofibrate modifies human vascular smooth muscle proteoglycans and reduces lipoprotein binding

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