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Intracellular matrix metalloproteinase-2 (MMP-2) regulates human platelet activation via hydrolysis of talin
Journal article   Peer reviewed

Intracellular matrix metalloproteinase-2 (MMP-2) regulates human platelet activation via hydrolysis of talin

Gerald Soslau, Christopher Mason, Stephen Lynch, James Benjamin, Dani Ashak, Jamunabai M. Prakash, Andrew Moore, Pamela Bagsiyao, Trevine Albert, Lynn M. Mathew, …
Thrombosis and haemostasis, v 111(1)
01 Jan 2014
PMID: 24136115

Abstract

Cardiovascular System & Cardiology Hematology Life Sciences & Biomedicine Peripheral Vascular Disease Science & Technology
Matrix metalloproteinase (MMP) activity is generally associated with 1 normal or pathological extracellular processes such as tissue remodelling in growth and development or in tumor metastasis and angiogenesis. Platelets contain at least three MMPs, 1, 2 and 9 that have been reported to stimulate or inhibit agonist-induced platelet aggregation via extracellular signals. The non-selective Zn+2 chelating MMP inhibitor, 1,10-phenanthroline, and the serine protease inhibitor, AEBSF, were found to inhibit all tested agonist-induced platelet aggregation reactions. In vitro analysis demonstrated that 1,10-phenanthroline completely inhibited MMP-1,2,and 9 but had little to no effect on calpain activity while the converse was true with AEBSF. We now demonstrate that MMP-2 functions intracellularly to regulate agonist-induced platelet aggregations via the hydrolytic activation of talin, the presumed final activating factor of glycoprotein (GP)IIb/IIIa integrin (the inside-out signal). Once activated GPIIb/IIIa binds the dimeric fibrinogen molecule required for platelet aggregation. The active intracellular MMP-2 molecule is complexed with JAK 2/STAT 3, as demonstrated by the fact that all three proteins are co-immunoprecipitated with either anti-JAK 2, or anti-STAT 3 antibodies and by immunofluorescence studies. The MMP-2 platelet activation pathway can be synergistically inhibited with the non-selective MMP inhibitor, 1,10-phenanthroline, plus a JAK 2 inhibitor. This activation pathway is distinct from the previously reported calpain-talin activating pathway. The; identification of a new central pathway for platelet aggregation presents new potential targets for drug regulation and furthers our understanding of the complexity of platelet activation mechanisms.

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Web of Science research areas
Hematology
Peripheral Vascular Disease
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