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Tenascin‐C triggers fibrin accumulation by downregulation of tissue plasminogen activator
Author(s) -
Brellier Florence,
Hostettler Katrin,
Hotz Hans-Rudolf,
Ozcakir Ceyda,
Çöloğlu Sedat A.,
Togbe Dieudonnée,
Ryffel Bernard,
Roth Michael,
Chiquet-Ehrismann Ruth
Publication year - 2011
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2011.02.023
Subject(s) - tenascin c , tenascin , fibrin , downregulation and upregulation , microbiology and biotechnology , tissue plasminogen activator , chemistry , plasminogen activator , activator (genetics) , biology , cancer research , fibronectin , immunology , biochemistry , gene , extracellular matrix , endocrinology
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.