Glycated Albumin and Pathological Shear Stress Alters Endothelial Cell Thrombogenic Potential, Pro-Inflammatory State and Cytoskeletal Dynamics

Maria, Zahra; Rubenstein, David A.

doi:10.4172/2155-6156.s4-003

Cited by 5 publications

(16 citation statements)

References 37 publications

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“…In general, we observed an increased surface expression of these two markers when endothelial cells were incubated with irreversibly glycated albumin (in the range of 20% for all conditions). [4][5][6] There has been no consensus on the expression of these two markers; some groups have observed an up-regulation, while others have observed a down-regulation of these markers. The expression profile appears to be very highly dependent on the cell type and the conditions studied.…”

Section: Connexin-43 and Caveolin-1 Expressionmentioning

confidence: 99%

“…In our previous work, we typically observed a significantly enhanced inflammatory response, via an increased ICAM-1 expression (average of ~80% increase for static conditions and > 100% increase for shear conditions), coupled with an increased thrombotic response, via an increased tissue factor expression (average of ~60% increase for static conditions and > 100% increase for shear conditions) and a decreased thrombomodulin expression (average of ~30% decrease for static conditions and a ~50% decrease for shear conditions). [4][5][6] In our previous work, this was especially prevalent for irreversibly glycated albumin. In cell culture experiments, others have also reported an enhanced ICAM-1 expression, an enhanced thrombogenicity and a decreased thrombomodulin expression, in response to glycated albumin.…”

Section: Endothelial Cell Inflammatory/thrombotic Markersmentioning

confidence: 99%

“…In all of our previous works, which investigated the role of glycation reversibility in endothelial cell metabolic activity, the metabolic activity of endothelial cells was altered in response to irreversibly glycated albumin (general decrease of ~50%) and/or shear stress (general increase of ~30%). [4][5][6] Other groups have observed altered endothelial cell metabolic activity, quantified by oxidative indicators, in response to glycated albumin. 12 Additionally, glycated low-density lipoprotein has also been shown to alter endothelial cell metabolic activity in culture.…”

Section: Endothelial Cell Metabolic Activitymentioning

confidence: 99%

“…This is especially prevalent for endothelial cell metabolic activity, viability, expression of ICAM-1, tissue factor and thrombomodulin and shear-induced cytoskeletal dynamics. [4][5][6] Here, we aimed to extend this work by including possible cross-talk between platelets and endothelial cells.…”

Section: Introductionmentioning

confidence: 99%

“…In previous work, we have examined the role of glycation extent on platelet or endothelial cell function and in general observed an increased thrombotic/inflammatory response after irreversibly glycated albumin exposure but not for reversibly glycated albumin. [4][5][6]9 Here, we examine the inflammatory and thrombogenic potential of endothelial cells and platelets concurrently exposed to AGEs glycated to various extents. We hypothesized that irreversibly glycated AGEs would elicit a more robust response than paired non-glycated proteins and reversibly glycated AGEs.…”

Section: Introductionmentioning

confidence: 99%

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Combined incubation of platelets and endothelial cells with glycated albumin: Altered thrombogenic and inflammatory responses

Rubenstein

Maria

2014

Diabetes and Vascular Disease Research

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Diabetes mellitus is a salient risk factor for the development of cardiovascular diseases (CVDs). Part of this risk is associated with the presence of advanced glycation end products (AGEs), which have been shown to up-regulate platelet or endothelial cell inflammatory and thrombogenic responses that are associated with CVDs. However, platelets perform mechanisms that alter endothelial cell inflammatory and thrombogenic responses, and endothelial cells perform similar mechanisms on platelets. Thus, our goal was to evaluate platelet and endothelial cell inflammatory and thrombogenic reactions that AGEs elicit during concurrent exposure. Endothelial cells were incubated with AGEs for 5 days, after which platelets were added. A time course for CVD inflammatory and thrombogenic responses was quantified as a function of extent of glycation. In general, the presence of platelets reduced AGE-induced endothelial cell responses associated with CVD progression and the presence of endothelial cells reduced platelet adhesion and activation responses, as compared with individual exposures. In general, the presence of irreversibly glycated albumin promoted CVD development to a greater extent than reversibly glycated albumin. This suggests that under diabetic conditions, platelets and endothelial cells can negatively feedback on each other, likely via enhanced adhesion, to elicit a reduced response associated with CVD progression.

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Section: Connexin-43 and Caveolin-1 Expressionmentioning

confidence: 99%

Section: Endothelial Cell Inflammatory/thrombotic Markersmentioning

confidence: 99%