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Project 81 Epidemiological approach of the interaction between inflammation and platelet activation in atherothrombosis
Onderzoekslijn AACD: Applied analytics of clinical data
Omschrijving Atherothrombosis is the major cause of death in developed countries. The pathophysiology of atherothrombosis is characterised by a chronic period of atherosclerosis progression, which may abruptly end with thrombotic occlusion of the damaged artery. Inflammation and platelet activation are both independent determinants of acute thrombotic occlusion of arteries, but little is known about the interaction between those two processes.

We have shown that:
- the density of the platelet collagen receptor (alpha2b1) on the platelet membrane is partly genetically determined by a 807 C/T single nucleotide polymorphism in the alpha2b1 gene and that high density of alpha2b1 on the platelet surface was associated with increased adhesion to collagen (1). Those outcomes were found in a study consisting of 30 healthy volunteers (1)
- women with genetic make-up for high alpha2b1 density on the platelet membrane (807 T homozygotes) had an increased risk of cardiovascular mortality if they were smokers, had diabetes or microalbuminuria. Those observations were done in a large cohort study of 12,239 women (2).
- prothrombotic make-up (blood group none-0, high vWF levels and high fibrinogen levels) was associated with increased acute ischaemic heart disease (IDH) incidence in women. This was investigated in a more recent cohort study among 17,500 women (3).

The ongoing projects focus on the actions of platelet activation markers to atherothrombosis. This will be investigated in several populations including: Haemodialysis patients (Necosad), a population of cardiology patients from Verona, Italy. Genetic markers of platelet thrombus formation will be determined with a novel genotyping method called: 'infrared Fluorescence Allele Specific Hybridization (iFLASH). We are developing a high througput facility to measure markers of platelet activation (e.g. soluble glycoprotein V, soluble GPIb, soluble GPVI, platelet factor 4, CD154, active vWF), prothrombotic markers (e.g. vWF and fibrinogen) and markers of inflammation (e.g. hs-CRP, IL-6, IL-10, IL-18, MPO, sICAM) using semi-automated high throughput ELISA's.
Projectleider Prof.dr. W.W.(Wouter) van Solinge
Instituut Universitair Medisch Centrum Utrecht locatie AZU Utrecht
Trefwoorden
Status Afgesloten
Periode 1-2006 - 1-2016
Partners Dr. R. Fijnheer, Jeroen Bosch Hospital, Den Bosch, the Netherlands
Dr. N. Martinelli, University of Verona, Verona, Italy
Dr. E. Boesschoten, Hans Mak Institute, Naarden, the Netherlands
Dr. B. van Jaarsveld, Dianed, Utrecht, the Netherlands
Medewerkers Ing. A.D. Barendrecht, technician

Financiering 1e Geldstroom - Intern

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