Literature DB >> 21354146

Tenascin-C triggers fibrin accumulation by downregulation of tissue plasminogen activator.

Florence Brellier1, Katrin Hostettler, Hans-Rudolf Hotz, Ceyda Ozcakir, Sedat A Çöloğlu, Dieudonnée Togbe, Bernard Ryffel, Michael Roth, Ruth Chiquet-Ehrismann.   

Abstract

We explored novel functions of tenascin-C by comparing mouse embryonic fibroblasts (MEFs) proficient or deficient in tenascin-C expression. Transcript profiling analysis identified tissue plasminogen activator (tPA) as the most consistently over-expressed gene in all tenascin-C deficient MEFs. This was confirmed by real-time PCR as well as by protein expression analysis. In agreement with these observations, tenascin-C deficient MEFs had an increased capacity to digest fibrin in situ. Consistently, tenascin-C expression in vivo was found to correlate with fibrin deposition in several diseases associated with tenascin-C overexpression such as fibrosis, asthma and cancer. In conclusion, the present study suggests a new role of tenascin-C as a regulator of the fibrinolytic system.
Copyright © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

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Year:  2011        PMID: 21354146     DOI: 10.1016/j.febslet.2011.02.023

Source DB:  PubMed          Journal:  FEBS Lett        ISSN: 0014-5793            Impact factor:   4.124


  13 in total

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