2014
DOI: 10.1189/jlb.0513262
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Involvement of fibrinolytic regulators in adhesion of monocytes to vascular endothelial cells induced by glycated LDL and to aorta from diabetic mice

Abstract: Diabetes mellitus accelerates the development of atherosclerotic cardiovascular diseases. Monocyte adhesion is an early cellular event of atherogenesis. Elevated levels of glyLDL were common in diabetic patients. Our previous studies indicated that HSF1 and p22-phox (a subunit of the NOX complex) were involved in glyLDL-induced up-regulation of PAI-1 in vascular EC. The present study demonstrated that glyLDL significantly increased the adhesion of monocytes to the surface of cultured human umbilical vein or PA… Show more

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Cited by 18 publications
(28 citation statements)
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“…These results were confirmed by other groups, who reported that gLDLs increase the oxidative stress in cultured EC by stimulating the RAGE/NADPH oxidase axis [44,71]. Recent studies [44,45,72] show that stimulation of the oxidative stress was followed by the upregulation of the pro-thrombotic PAI-1 or of various pro-inflammatory proteins (C reactive protein, MCP-1, VCAM-1) that exacerbate the inflammatory state and stimulate monocyte adhesion to EC (Figure 3a).…”
Section: Upregulation Of the Main Ec Pro-oxidant Proteins By Glpsupporting
confidence: 84%
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“…These results were confirmed by other groups, who reported that gLDLs increase the oxidative stress in cultured EC by stimulating the RAGE/NADPH oxidase axis [44,71]. Recent studies [44,45,72] show that stimulation of the oxidative stress was followed by the upregulation of the pro-thrombotic PAI-1 or of various pro-inflammatory proteins (C reactive protein, MCP-1, VCAM-1) that exacerbate the inflammatory state and stimulate monocyte adhesion to EC (Figure 3a).…”
Section: Upregulation Of the Main Ec Pro-oxidant Proteins By Glpsupporting
confidence: 84%
“…Interestingly, exposure of EC to nLDL in HG culture medium compared to normal glucose determines the stimulation of RAGE and NADPH subunits (p22phox, NOX4, and p67phox), supporting the concerted pathogenic potential of hyperglycemia and dyslipidemia in T2DM patients [70]. These results were confirmed by other groups, who reported that gLDLs increase the oxidative stress in cultured EC by stimulating the RAGE/NADPH oxidase axis [44,71]. Recent studies [44,45,72] show that stimulation of the oxidative stress was followed by the upregulation of the pro-thrombotic PAI-1 or of various pro-inflammatory proteins (C reactive protein, MCP-1, VCAM-1) that exacerbate the inflammatory state and stimulate monocyte adhesion to EC (Figure 3a).…”
Section: Upregulation Of the Main Ec Pro-oxidant Proteins By Glpsupporting
confidence: 67%
See 1 more Smart Citation
“…Fibrinolysis regulators are involved in adhesion of monocytes to endothelial cells in vitro . PAI-1 and uPA are required for GlyLDL-induced monocyte adhesion to endothelial cells 31 . Macrophages are highly heterogeneous cells that can adapt their functions in response to local microenvironmental signals.…”
Section: Discussionmentioning
confidence: 99%
“…The AGE–RAGE interaction is known to stimulate the activation of inflammatory pathways . Reports from our and other groups show that glycated LDL (gLDL) contribute to the progression of accelerated atherosclerosis in diabetes by determining the increased expression of RAGE, of vascular cell adhesion molecule 1 (VCAM‐1) and monocyte chemoattractant protein 1 (MCP‐1) expressions, thus inducing the adhesion of monocytes to activated human endothelial cells (HEC), through mechanisms mediated by oxidative and endoplasmic reticulum stress (ERS) .…”
Section: Introductionmentioning
confidence: 99%