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  • Title: Tenascin-C triggers fibrin accumulation by downregulation of tissue plasminogen activator.
    Author: Brellier F, Hostettler K, Hotz HR, Ozcakir C, Çöloğlu SA, Togbe D, Ryffel B, Roth M, Chiquet-Ehrismann R.
    Journal: FEBS Lett; 2011 Mar 23; 585(6):913-20. PubMed ID: 21354146.
    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.
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