Nonenzymatic glycation of human platelet membrane proteins in vitro and in vivo.

Sampietro, Tiziana; Lenzi, S; Cecchetti, P; Giampietro, Ottavio; Cruschelli, L; Navalesi, R.

doi:10.1093/clinchem/32.7.1328

Cited by 41 publications

(5 citation statements)

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“…Platelet proteins of T2DM patients were glycated to a higher extent, indicating that biochemical modification occurs despite the relatively short life span of platelets in circulation. These results are in agreement with previously published studies which show enhanced glycation of platelet membrane proteins in patients with diabetes [8,9].…”

Section: Characterization Of Activation Reactivity and Protein Glycation In Platelets From Diabetic Patientssupporting

confidence: 94%

Diabetes and Hyperglycemia Affect Platelet GPIIIa Expression: Effects on Adhesion Potential of Blood Platelets from Diabetic Patients under In Vitro Flow Conditions

Przygodzki

Luzak

Kassassir

et al. 2020

IJMS

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Blood platelets play a crucial role in the early stages of atherosclerosis development. The process is believed to require firm adhesion of platelets to atherosclerosis-prone sites of the artery. However, little evidence exists regarding whether the blood platelets of individuals with pathological conditions associated with atherosclerosis have higher potential for adhesion. This process is to a large extent dependent on receptors present on the platelet membrane. Therefore, the aim of the presented study was to determine whether blood platelets from diabetic patients have higher capacity of adhesion under flow conditions and how diabetes affects one of the crucial platelet receptors involved in the process of adhesion—GPIIIa. The study compares the ability of platelets from non-diabetic and diabetic humans to interact with fibrinogen and von Willebrand factor, two proteins found in abundance on an inflamed endothelium, under flow conditions. The activation and reactivity of the blood platelets were also characterized by flow cytometry. Platelets from diabetic patients did not demonstrate enhanced adhesion to either studied protein, although they presented increased basal activation and responsiveness towards low concentrations of agonists. Platelets from diabetic patients were characterized by lower expression of GPIIIa, most likely due to an enhanced formation of platelet-derived microparticles PMPs, as supported by the observation of elevated concentration of this integrin and of GPIIIa-positive PMPs in plasma. We conclude that altered functionality of blood platelets in diabetes does not increase their adhesive potential. Increased glycation and decrease in the amount of GPIIIa on platelets may be partially responsible for this effect. Therefore, higher frequency of interactions of platelets with the endothelium, which is observed in animal models of diabetes, is caused by other factors. A primary cause may be a dysfunctional vascular wall.

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Section: Characterization Of Activation Reactivity and Protein Glycation In Platelets From Diabetic Patientssupporting

confidence: 94%

Diabetes and Hyperglycemia Affect Platelet GPIIIa Expression: Effects on Adhesion Potential of Blood Platelets from Diabetic Patients under In Vitro Flow Conditions

Przygodzki

Luzak

Kassassir

et al. 2020

IJMS

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“…Platelets from people with diabetes have reduced membrane fluidity that is thought to be related to membrane cholesterol to phospholipid ratio [61]. Another process that likely contributes to enhanced platelet aggregation is an increase in glycation of platelet membrane proteins [67].…”

Section: Pathophysiology Of Diabetic Vasculopathymentioning

confidence: 99%

Diabetes‐associated macrovasculopathy: pathophysiology and pathogenesis

Rahman¹,

Rahman

Ismail

et al. 2006

Diabetes Obesity Metabolism

219

166

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The complications associated with diabetic vasculopathy are commonly grouped into two categories: microvascular and macrovascular complications. In diabetes, macrovascular disease is the commonest cause of mortality and morbidity and is responsible for high incidence of vascular diseases such as stroke, myocardial infarction and peripheral vascular diseases. Macrovascular diseases are traditionally thought of as due to underlying obstructive atherosclerotic diseases affecting major arteries. Pathological changes of major blood vessels leading to functional and structural abnormalities in diabetic vessels include endothelial dysfunction, reduced vascular compliance and atherosclerosis. Besides, advanced glycation end product formation interacts with specific receptors that lead to overexpression of a range of cytokines. Haemodynamic pathways are activated in diabetes and are possibly amplified by concomitant systemic hypertension. Apart from these, hyperglycaemia, non-enzymatic glycosylation, lipid modulation, alteration of vasculature and growth factors activation contribute to development of diabetic vasculopathy. This review focuses on pathophysiology and pathogenesis of diabetes-associated macrovasculopathy.

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“…Increased platelet membrane cholesterol to phospholipid content is, in turn, associated with increased platelet [Ca2+Ii responses to agonists (20,189,190,261). Another mechanism that appears to contribute to enhanced platelet [Ca2+Ii responses, aggregation, and release reactions (70,205,393) in patients with diabetes mellitus is the increased nonenzymatic glycosylation of platelet membrane proteins (340), which decreases membrane fluidity and enhances the [Ca2+],, aggregation, and release responses to agonists (205,243,269,309,339,358,436). Resistance to the normal actions of insulin as occurs in hypertension and NIDDM (1 17,308,368,370,372,374, 377) could also potentially contribute to enhanced [Ca2 'Ii increases and associated hyperaggregation (205,397) and release (205), as insulin has been observed to attenuate platelet [Ca2 'Ii and aggregation responses (123,412) (similar to effects seen in VSMC (174,202,278,3 14)).…”

Section: Picitelet Adhesion and Platelet Aggregationmentioning

confidence: 99%