Literature DB >> 21435699

Decreased phosphorylation of platelet vasodilator-stimulated phosphoprotein in periodontitis--a role of periodontal pathogens.

Markus Laky1, Alice Assinger, Azadeh Esfandeyari, Kristina Bertl, Hady Haririan, Ivo Volf.   

Abstract

INTRODUCTION: Epidemiological studies indicate an association between periodontitis and cardiovascular disease, but the underlying mechanisms are poorly understood. Vasodilator-stimulated phosphoprotein (VASP) in its phosphorylated form represents a regulator of platelet function and an indicator for the sensitivity of platelets towards physiologically relevant antagonists of platelet function. As platelets and their activation state play a central role in the development of cardiovascular disease, this study aimed to investigate the influence of periodontal disease and periodontal pathogens on intraplatelet VASP-phosphorylation and platelet function.
MATERIAL AND METHODS: Besides several markers of platelet activation, basal and PGE(1) induced intracellular VASP-phosphorylation were determined in platelets of periodontitis patients (n = 26) and healthy donors (n = 19). Furthermore, platelets from healthy donors were incubated with distinct periodontal pathogens and basal and PGE(1) induced VASP-phosphorylation was determined.
RESULTS: Compared to controls, platelets of periodontitis patients showed a significant decrease in basal and PGE(1) induced VASP-phosphorylation. VASP-phosphorylation in platelets from periodontitis patients positive for Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis or Tannerella forsythia was significantly decreased compared to patients that were negative for these bacteria. Furthermore, VASP-phosphorylation in platelets isolated from healthy donors was affected by incubation with these periodontal pathogens.
CONCLUSIONS: Our results provide evidence that periodontitis interferes with VASP-phosphorylation in human platelets, presumably as a consequence of a direct effect of periodontitis-associated bacteria. Decreased basal and PGE(1) induced VASP-phosphorylation might represent a mechanism responsible for enhanced platelet activation in periodontitis.
Copyright © 2011 Elsevier Ltd. All rights reserved.

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Year:  2011        PMID: 21435699     DOI: 10.1016/j.thromres.2011.02.016

Source DB:  PubMed          Journal:  Thromb Res        ISSN: 0049-3848            Impact factor:   3.944


  2 in total

1.  Laropiprant attenuates EP3 and TP prostanoid receptor-mediated thrombus formation.

Authors:  Sonia Philipose; Viktoria Konya; Mirjana Lazarevic; Lisa M Pasterk; Gunther Marsche; Sasa Frank; Bernhard A Peskar; Akos Heinemann; Rufina Schuligoi
Journal:  PLoS One       Date:  2012-08-01       Impact factor: 3.240

2.  Periodontal treatment does not result in detectable platelet activation in vivo.

Authors:  Markus Laky; Isabella Anscheringer; Lukas Wolschner; Stefan Heber; Hady Haririan; Xiaohui Rausch-Fan; Ivo Volf; Andreas Moritz; Alice Assinger
Journal:  Clin Oral Investig       Date:  2019-08-29       Impact factor: 3.573

  2 in total

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