Involvement of the glycoproteic lb-V-IX complex in nickel-induced platelet activation

Sivia Riondino, Fabio Maria Pulcinelli, Pasquale Pignatelli, Pier Paolo Gazzaniga

Research output: Contribution to journalArticlepeer-review


We studied the effect of nickel ions on platelet function because hypernickelemia has been found in patients with acute myocardial infarction. We previously demonstrated that nickel can activate an intracellular pathway leading to cytoskeleton reorganization consequent to tyrosine phosphorylation of p60 src in human platelets independently of integrin alpha-IIb-beta 3 (αIIbβ3). Moreover, in von Willebrand factor-stimulated platelets, the tyrosine phosphorylation of pp60 csrc is closely associated with the activation of phosphatidylinositol 3-kinase (PIK), and two adhesion receptors, glycoprotein (Gp)Ib and GpIIb/IIIa (αIIbβ3), are involved. In our study, 1 and 5 mM nickel in the presence of fibrinogen induced platelet aggregation (independently of protein kinase C activation) and secretion. The pretreatment with a PIK inhibitor, wortmannin, strongly decreased nickel-induced platelet aggregation. Platelet treatment with mocarhagin, a cobra venom metalloproteinase that cleaves GpIba, significantly reduced aggregation induced by 5 mM without affecting the response to other agonists such as adenosine diphosphate (ADP). Moreover, nickel caused PIK translocation to the cytoskeleton. Taken together, these observations suggest a partial involvement of both integrins αIIbβ3 and GpIb-V-IX complex in Ni 2+-induced platelet activation.

Original languageEnglish
Pages (from-to)225-228
Number of pages4
JournalEnvironmental Health Perspectives
Issue number3
Publication statusPublished - 2001


  • Adhesion receptors
  • Integrins
  • Nickel
  • Platelet activation

ASJC Scopus subject areas

  • Environmental Science(all)
  • Environmental Chemistry
  • Public Health, Environmental and Occupational Health

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