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

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Title: Tenascin-C triggers fibrin accumulation by downregulation of tissue plasminogen activator
Authors: Brellier, Florence1 florence.brellier@fmi.ch, Hostettler, Katrin2, Hotz, Hans-Rudolf1, Ozcakir, Ceyda3, Çöloğlu, Sedat A.4, Togbe, Dieudonnée5, Ryffel, Bernard5, Roth, Michael2, Chiquet-Ehrismann, Ruth1
Source: FEBS Letters. Mar2011, Vol. 585 Issue 6, p913-920. 8p.
Subjects: Tenascin, Fibrin, Tissue plasminogen activator, Extracellular matrix, Fibroblasts, Laboratory mice, Polymerase chain reaction, Gene expression, Fibrosis, Asthma, Cancer
Abstract: 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 &y& Elsevier]
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Database: Engineering Source
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Abstract: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 &y& Elsevier]
ISSN:00145793
DOI:10.1016/j.febslet.2011.02.023