Journal
BIOCHIMIE
Volume 95, Issue 6, Pages 1252-1257Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biochi.2013.01.021
Keywords
Platelet aggregation; Wnt signalling; Protein kinase C; Proteasome; Calpain; Thrombin
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Funding
- Department of Biotechnology (DBT)
- Department of Science and Technology (DST), Government of India
- Council of Scientific & Industrial Research (CSIR)
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The Wnt/beta-catenin pathway controls developmental processes and homeostasis; however, abnormal activation of this pathway has been linked to several human diseases. Recent reports have demonstrated regulation of platelet function by canonical and non-canonical Wnt signalling. Platelet aggregation plays a crucial role in haemostasis and thrombosis. Here we report for the first time that, induction of sustained aggregation of platelets by a strong agonist in the presence of calcium was associated with nearly complete proteolysis of beta-catenin, which was abrogated upon depletion of calcium from platelet suspension. beta-catenin cleavage was disallowed in absence of aggregation, thus implicating integrin alpha(IIb)beta(3) engagement in beta-catenin proteolysis. Degradation of beta-catenin was blocked partially by inhibitors of either proteasome or calpain and completely when cells were exposed to both the inhibitors. Protein kinase C inhibition, too, abolished beta-catenin degradation. Thus activities of proteasome, calpain and protein kinase C regulate stabilization of beta-catenin in aggregated human platelets. (C) 2013 Elsevier Masson SAS. All rights reserved.
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