Literature DB >> 22104553

Matrix metalloproteinase-10 effectively reduces infarct size in experimental stroke by enhancing fibrinolysis via a thrombin-activatable fibrinolysis inhibitor-mediated mechanism.

J Orbe1, J Barrenetxe, J A Rodriguez, D Vivien, C Orset, W C Parks, T P Birkland, R Serrano, A Purroy, S Martinez de Lizarrondo, E Angles-Cano, J A Páramo.   

Abstract

BACKGROUND: The fibrinolytic and matrix metalloproteinase (MMP) systems cooperate in thrombus dissolution and extracellular matrix proteolysis. The plasminogen/plasmin system activates MMPs, and some MMPs have been involved in the dissolution of fibrin by targeting fibrin(ogen) directly or by collaborating with plasmin. MMP-10 has been implicated in inflammatory/thrombotic processes and vascular integrity, but whether MMP-10 could have a profibrinolytic effect and represent a promising thrombolytic agent is unknown. METHODS AND
RESULTS: The effect of MMP-10 on fibrinolysis was studied in vitro and in vivo, in MMP-10-null mice (Mmp10(-/-)), with the use of 2 different murine models of arterial thrombosis: laser-induced carotid injury and ischemic stroke. In vitro, we showed that MMP-10 was capable of enhancing tissue plasminogen activator-induced fibrinolysis via a thrombin-activatable fibrinolysis inhibitor inactivation-mediated mechanism. In vivo, delayed fibrinolysis observed after photochemical carotid injury in Mmp10(-/-) mice was reversed by active recombinant human MMP-10. In a thrombin-induced stroke model, the reperfusion and the infarct size in sham or tissue plasminogen activator-treated animals were severely impaired in Mmp10(-/-) mice. In this model, administration of active MMP-10 to wild-type animals significantly reduced blood reperfusion time and infarct size to the same extent as tissue plasminogen activator and was associated with shorter bleeding time and no intracranial hemorrhage. This effect was not observed in thrombin-activatable fibrinolysis inhibitor-deficient mice, suggesting thrombin-activatable fibrinolysis inhibitor inactivation as one of the mechanisms involved in the MMP-10 profibrinolytic effect.
CONCLUSIONS: A novel profibrinolytic role for MMP-10 in experimental ischemic stroke is described, opening new pathways for innovative fibrinolytic strategies in arterial thrombosis.

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Year:  2011        PMID: 22104553     DOI: 10.1161/CIRCULATIONAHA.111.047100

Source DB:  PubMed          Journal:  Circulation        ISSN: 0009-7322            Impact factor:   29.690


  22 in total

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Journal:  ACS Med Chem Lett       Date:  2018-04-16       Impact factor: 4.345

2.  Temporal analysis of blood-brain barrier disruption and cerebrospinal fluid matrix metalloproteinases in rhesus monkeys subjected to transient ischemic stroke.

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3.  MMP10 Promotes Efficient Thrombolysis After Ischemic Stroke in Mice with Induced Diabetes.

Authors:  Manuel Navarro-Oviedo; Carmen Roncal; Agustina Salicio; Miriam Belzunce; Obdulia Rabal; Estefanía Toledo; Beatriz Zandio; Jose A Rodríguez; Jose A Páramo; Roberto Muñoz; Josune Orbe
Journal:  Transl Stroke Res       Date:  2018-07-27       Impact factor: 6.829

4.  Matrix metalloproteinase-10 plays an active role in microvascular complications in type 1 diabetic patients.

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Review 6.  Matrix metalloproteinases in kidney homeostasis and diseases.

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8.  Genetic variations within metalloproteinases impact on the prophylaxis of depressive phases in bipolar patients.

Authors:  Antonio Drago; Barbara Monti; Diana De Ronchi; Alessandro Serretti
Journal:  Neuropsychobiology       Date:  2014-02-27       Impact factor: 2.328

9.  Matrix metalloproteinase 10 gene polymorphism and atherothrombotic cerebral infarction risk in a Han Chinese population.

Authors:  Feng Zhu; Xiao-Ping Jin; Min Zhu; Ling-Ling Zhang; Feng Wang; Wan-Fen Wang; Xiao-Fei Hu; Wei-Ling Li; Cai Li; Zhou Zheng
Journal:  Int J Clin Exp Med       Date:  2013-08-01

10.  A pharmacogenomic profile of human neural progenitors undergoing differentiation in the presence of the traditional Chinese medicine NeuroAiD.

Authors:  H Y A Chan; L W Stanton
Journal:  Pharmacogenomics J       Date:  2016-04-05       Impact factor: 3.550

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