Advanced protein glycosylation induces transendothelial human monocyte chemotaxis and secretion of platelet-derived growth factor: role in vascular disease of diabetes and aging.

Kirstein, Martina; Brett, Jerold; Radoff, Steven; Ogawa, Satoshi; Stern, David M.; Vlassara, Helen

doi:10.1073/pnas.87.22.9010

Cited by 341 publications

(155 citation statements)

References 24 publications

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“…It is possible that human SMCs are quite resistant to increased oxidative stress, which mediates the effects of AGE-RAGE interaction in endothelial cells and monocytes/macrophages [46]. Therefore, direct effects of AGEs and S100 peptides on endothelial cells [13,47] and/or monocytes/macrophages [48,49] might be more pronounced than their effects on SMCs.…”

Section: Rage Ligands Do Not Stimulate Human Smc Proliferationmentioning

confidence: 99%

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

et al. 2003

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Aims/hypothesis. Diabetes 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. Methods. Primary 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. Results. Human arterial smooth muscle cells express the receptor for advanced glycation end-products, but its ligands N ε -(carboxymethyl)lysine-modified proteins, methylglyoxal-modified proteins, S100B polypeptide and amyloid-β (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/interpretation. Oleate, 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. [Diabetologia (2003[Diabetologia ( ) 46:1676[Diabetologia ( -1687 Keywords Atherosclerosis, diabetes, diacylglycerol, fatty acids, platelet-derived growth factor, phospholipase D, triglycerides. Atherosclerosis is accelerated by both Type I and Type 2 diabetes [1] by mechanisms that are poorly understood. Proliferation of arterial smooth muscle cells (SMCs) in lesions of atherosclerosis plays an important role in progression of early fatty streaks to fibroatheromas. We have recently reported that increased SMC proliferation in fibroatheromas occurs concomitantly with hyperglycaemia and an increased plasma triglyceride concentration in a porcine model of diabetes-accelerated atherosclerosis [2]. However, increased plasma glucose concentrations do not directly stimulate proliferation of SMCs isolated from these animals or from human subjects [2]. In this study, we investigated advanced glycation end-products (AGEs)

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Section: Rage Ligands Do Not Stimulate Human Smc Proliferationmentioning

confidence: 99%

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

et al. 2003

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“…A syndrome of insulin resistance, central obesity, hypertension and dyslipidaemia, also known as the metabolic syndrome, may constitute these common precursors. Evidence from an increasing number of basic research studies points to a causal role of oxidative stress and inflammatory processes in the aetiology of type 2 diabetes and the metabolic syndrome [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Circulating oxidised low-density lipoprotein and intercellular adhesion molecule-1 and risk of type 2 diabetes mellitus: the Atherosclerosis Risk in Communities Study

et al. 2006

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Aims/hypothesis To evaluate the role of oxidative stress and inflammation in the aetiology of type 2 diabetes, we examined the association of oxidised LDL (ox-LDL) and soluble intercellular adhesion molecule-1 (sICAM-1) levels with type 2 diabetes incidence over 9 years in the Atherosclerosis Risk in Communities Study. Materials and methods In a large, prospective, case-cohort design, ox-LDL and sICAM-1 were measured in stored plasma samples collected at baseline in stratified samples of 581 diabetes cases and 572 non-cases selected from 10,275 middle-aged men and women without prevalent diabetes at baseline. Results Compared with non-cases, diabetes cases had significantly higher mean baseline levels of ox-LDL and sICAM-1. Elevated ox-LDL and sICAM-1 were both associated with increased risk of incident diabetes after adjustment for age, sex, race and centre, with hazard ratios for the highest vs lowest tertiles of 1.68 (95% CI 1.25-2.24) and 1.91 (95% CI 1.45-2.50), respectively. After additional adjustment for fasting glucose, waist circumference, HDL-cholesterol, triacylglycerol, hypertension and C-reactive protein, only sICAM-1 remained an independent predictor of incident diabetes (hazard ratio 1.50; 95% CI 1.02-2.23). Conclusions/interpretation In this community-based cohort of middle-aged US adults, elevated plasma ox-LDL and sICAM-1 levels were associated with increased risk of type 2 diabetes. Measurement of ICAM-1 or ox-LDL, or other measures related to inflammation or oxidative stress, may be helpful in identifying those patient populations in which to test whether novel therapies that inhibit specific pathways related to inflammation or oxidative stress are beneficial in the prevention of diabetes in humans.

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“…Studies in vitro have shown that AGE can mediate monocytic chemotactic activity [6], and block the cytostatic effect of nitric oxide-dependent vasodilatation [7]. AGE modification of mesangial cell matrix has been reported to alter the mesangial proliferative response [8].…”

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confidence: 99%

Toxic action of advanced glycation end products on cultured retinal capillary pericytes and endothelial cells: relevance to diabetic retinopathy

et al. 1997

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Summary The toxic effects of advanced glycation end products (AGEs) on bovine retinal capillary pericytes (BRP) and endothelial cells (BREC) were studied. AGE-modified bovine serum albumin (AGE-BSA) was toxic to BRP. At a concentration of 500 m g/ml it reduced the BRP number to 48 ± 3 % (p < 0.05) of untreated controls, as determined by cell counting with haemocytometer. AGE-BSA was also toxic to bovine aortic endothelial cells (BAEC) reducing cell number to 84 ± 3.1 % of untreated controls. Under similar conditions, low concentrations (62.5 m g/ml) of AGE-BSA were mitogenic to BREC increasing the cell proliferation to 156 ± 11 % (p < 0.05) above that of untreated controls. At a higher dose of 500 m g/ml AGE-BSA decreased the proliferation of BREC to 85 ± 6 % of untreated controls. Immunoblot analysis demonstrated that BRP and BREC express the p60 AGE-receptor. Retinal capillary bed from the human also stained positively for the p60 AGE-receptor. Addition of 0.25 m g/ml of p60 AGE-receptor antibody was able to block the effects of AGE-BSA on BRP and BREC. The level of binding of [ 125 I]-labelled AGE-BSA to the cell surface was small but significant among the three cell types. There was also an increase in the internalized pool of radioligand in BRP and BREC but this was very much lower than in BAEC. In all the cell types the internalized pool of [ 125 I]-labelled AGE-BSA was much larger than the amount associated with the cell surface. Degradation products were not detected in the media over the 24-h incubation of the cells with [ 125 I]AGE-BSA. The binding of [ 125 I]-labelled AGE-BSA to the cell surface was prevented by the addition of p60 AGE-receptor. These results suggest that the interaction of AGE-modified proteins with the membrane-bound AGE-receptor may play an important role in the pathogenesis of diabetic retinopathy. [Diabetologia (1997) 40: 156-164]

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Advanced protein glycosylation induces transendothelial human monocyte chemotaxis and secretion of platelet-derived growth factor: role in vascular disease of diabetes and aging.

Cited by 341 publications

References 24 publications

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

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

Circulating oxidised low-density lipoprotein and intercellular adhesion molecule-1 and risk of type 2 diabetes mellitus: the Atherosclerosis Risk in Communities Study

Toxic action of advanced glycation end products on cultured retinal capillary pericytes and endothelial cells: relevance to diabetic retinopathy

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