Irreversibly glycated LDL induce oxidative and inflammatory state in human endothelial cells; added effect of high glucose

Toma, Laura; Stancu, Camelia S.; Botez, Gabriela; Sima, Anca V.; Simionescu, Maya

doi:10.1016/j.bbrc.2009.10.066

Cited by 56 publications

(35 citation statements)

References 23 publications

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“…As known from the literatures, reactive oxygen species (ROS) can mediate high glucose-induced activation of protein kinase C and NFB dependent MCP-1 expression (Ha et al, 2008). High level of circulating MCP-1 can lead to the vascular inflammation via interacting with ox-LDL and finally enhance the proinflammatory state (Toma et al, 2009). Furthermore, the level of NFB is positive correlation with the levels of end-products from lipid peroxidation (Aragno et al, 2009).…”

Section: Discussionmentioning

confidence: 97%

Vascular protective potential of the total flavanol glycosides from Abacopteris penangiana via modulating nuclear transcription factor-κB signaling pathway and oxidative stress

Chen

Lei

et al. 2011

Journal of Ethnopharmacology

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Section: Discussionmentioning

confidence: 97%

Vascular protective potential of the total flavanol glycosides from Abacopteris penangiana via modulating nuclear transcription factor-κB signaling pathway and oxidative stress

Chen

Lei

et al. 2011

Journal of Ethnopharmacology

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“…13,14 AGEs increase the expression and activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in human endothelial cells, an important source of vascular oxidative stress in Type 2 diabetes. 15 Increased NADPH oxidase activity results in formation of free radicals and depletion of cellular antioxidants such as glutathione, glutathione peroxidase, superoxide dismutase and catalase. Free radical mediated lipid peroxidation of polyunsaturated fatty acids gives rise to formation of several reactive a-, b-unsaturated aldehydes such as 4-hydroxy-trans-2-nonenal (HNE), 4-oxotrans-2-nonenal (4-ONE), acrolein and 4-oxo-trans-2-hexanal, all of which are aldehydes such as glucose, and have the potential to be considered as biomarkers of glycaemic status but can also form advanced lipid peroxidation end products (ALE).…”

Section: 10mentioning

confidence: 99%

Oxidative stress in diabetes – circulating advanced glycation end products, lipid oxidation and vascular disease

Dias

Griffiths

2013

Ann Clin Biochem

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“…Activated H-Ras may stimulate ROS production by activating NOX (20,21). A recent study demonstrated that AGEs-LDL increased NOX activity in EC via RAGE (56). The abundance of NOX2 in EC was increased by glyLDL and reached a peak around 1 h. The activation of NOX increases the generation of ROS (21,28).…”

Section: Figmentioning

confidence: 99%

Involvement of RAGE, NADPH Oxidase, and Ras/Raf-1 Pathway in Glycated LDL-Induced Expression of Heat Shock Factor-1 and Plasminogen Activator Inhibitor-1 in Vascular Endothelial Cells

et al. 2010

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Atherothrombotic cardiovascular diseases are the predominant causes of mortality of diabetic patients. Plasminogen activator inhibitor-1 (PAI-1) is the major physiological inhibitor for fibrinolysis, and it is also implicated in inflammation and tissue remodeling. Increased levels of PAI-1 and glycated low-density lipoprotein (glyLDL) were detected in patients with diabetes. Previous studies in our laboratory demonstrated that heat shock factor-1 (HSF1) is involved in glyLDL-induced PAI-1 overproduction in vascular endothelial cells (EC). The present study investigated transmembrane signaling mechanisms involved in glyLDL-induced HSF1 and PAI-1 up-regulation in cultured human vascular EC and streptozotocin-induced diabetic mice. Receptor for advanced glycation end products (RAGE) antibody prevented glyLDL-induced increase in the abundance of PAI-1 in EC. GlyLDL significantly increased the translocation of V-Ha-Ras Harvey rat sarcoma viral oncogene homologue (H-Ras) from cytoplasm to membrane compared with LDL. Farnesyltransferase inhibitor-277 or small interference RNA against H-Ras inhibited glyLDL-induced increases in HSF1 and PAI-1 in EC. Treatment with diphenyleneiodonium, a nicotinamide adenine dinucleotide phosphate oxidase (NOX) inhibitor, blocked glyLDL-induced translocation of H-Ras, elevated abundances of HSF1 and PAI-1 in EC, and increased release of hydrogen peroxide from EC. Small interference RNA for p22 phox prevented glyLDL-induced expression of NOX2, HSF1, and PAI-1 in EC. GlyLDL significantly increased V-raf-1 murine leukemia viral oncogene homolog 1 (Raf-1) phosphorylation. Treatment with Raf-1 inhibitor blocked glyLDLinduced increase of PAI-1 mRNA in EC. The levels of RAGE, H-Ras, NOX4, HSF1, and PAI-1 were increased in hearts of streptozotocin-diabetic mice and positively correlated with plasma glucose. The results suggest that RAGE, NOX, and H-Ras/Raf-1 are implicated in the up-regulation of HSF1 or PAI-1 in vascular EC under diabetes-associated metabolic stress. (Endocrinology 151: 4455-4466, 2010)

show abstract

Irreversibly glycated LDL induce oxidative and inflammatory state in human endothelial cells; added effect of high glucose

Cited by 56 publications

References 23 publications

Vascular protective potential of the total flavanol glycosides from Abacopteris penangiana via modulating nuclear transcription factor-κB signaling pathway and oxidative stress

Vascular protective potential of the total flavanol glycosides from Abacopteris penangiana via modulating nuclear transcription factor-κB signaling pathway and oxidative stress

Oxidative stress in diabetes – circulating advanced glycation end products, lipid oxidation and vascular disease

Involvement of RAGE, NADPH Oxidase, and Ras/Raf-1 Pathway in Glycated LDL-Induced Expression of Heat Shock Factor-1 and Plasminogen Activator Inhibitor-1 in Vascular Endothelial Cells

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