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

被引：19

作者：

Brellier, Florence ^{[1
]}

Hostettler, Katrin ^{[2
]}

Hotz, Hans-Rudolf ^{[1
]}

Ozcakir, Ceyda ^{[3
]}

Cologlu, Sedat A. ^{[4
]}

Togbe, Dieudonnee ^{[5
,6
]}

Ryffel, Bernard ^{[5
,6
]}

Roth, Michael ^{[2
]}

Chiquet-Ehrismann, Ruth ^{[1
]}

机构：

[1] Novartis Res Fdn, Friedrich Miescher Inst Biomed Res, CH-4058 Basel, Switzerland

[2] Univ Basel Hosp, Clin Resp Med, CH-4031 Basel, Switzerland

[3] Yeditepe Univ, Fac Dent, Dept Oral & Maxillofacial Surg, Istanbul, Turkey

[4] Yeditepe Univ, Fac Med, Dept Pathol, Istanbul, Turkey

[5] Univ Orleans, Mol Immunol & Embryol UMR6218, Orleans, France

[6] CNRS, F-45071 Orleans, France

来源：

FEBS LETTERS | 2011年 / 585卷 / 06期

关键词：

Extracellular matrix; Tenascin; Tissue plasminogen activator; Fibrin; TUMOR STROMA GENERATION; GROWTH; DEFICIENCY; EXPRESSION; FIBROSIS; INDUCTION; MIGRATION; REVEALS; FAMILY; WOUNDS;

D O I：

10.1016/j.febslet.2011.02.023

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

引用

页码：913 / 920

页数：8

共 40 条

[1] TENASCIN DURING GUT DEVELOPMENT - APPEARANCE IN THE MESENCHYME, SHIFT IN MOLECULAR-FORMS, AND DEPENDENCE ON EPITHELIAL MESENCHYMAL INTERACTIONS [J].

AUFDERHEIDE, E ;

EKBLOM, P .

JOURNAL OF CELL BIOLOGY, 1988, 107 (06) :2341-2349

[2]

Bárdos H, 1998, THROMB HAEMOSTASIS, V80, P767

[3] Tenascins and their implications in diseases and tissue mechanics [J].

Brellier, F. ;

Tucker, R. P. ;

Chiquet-Ehrismann, R. .

SCANDINAVIAN JOURNAL OF MEDICINE & SCIENCE IN SPORTS, 2009, 19 (04) :511-519

[4] Coagulation factors in the airways in moderate and severe asthma and the effect of inhaled steroids [J].

Brims, F. J. H. ;

Chauhan, A. J. ;

Higgins, B. ;

Shute, J. K. .

THORAX, 2009, 64 (12) :1037-1043

[5]

BROWN LF, 1993, AM J PATHOL, V142, P273

[6] Loss of fibrinogen rescues mice from the pleiotropic effects of plasminogen deficiency [J].

Bugge, TH ;

Kombrinck, KW ;

Flick, MJ ;

Daugherty, CC ;

Danton, MJS ;

Degen, JL .

CELL, 1996, 87 (04) :709-719

[7] Airway remodeling and repair [J].

Busse, W ;

Elias, J ;

Sheppard, D ;

Banks-Schlegel, S .

AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1999, 160 (03) :1035-1042

[8] INVOLVEMENT OF THE PLASMIN SYSTEM IN DISSOCIATION OF THE INSULIN-LIKE GROWTH FACTOR-BINDING PROTEIN COMPLEX [J].

CAMPBELL, PG ;

NOVAK, JF ;

YANOSICK, TB ;

MCMASTER, JH .

ENDOCRINOLOGY, 1992, 130 (03) :1401-1412

[9] FIBRIN-II INDUCES ENDOTHELIAL-CELL CAPILLARY-TUBE FORMATION [J].

CHALUPOWICZ, DG ;

CHOWDHURY, ZA ;

BACH, TL ;

BARSIGIAN, C ;

MARTINEZ, J .

JOURNAL OF CELL BIOLOGY, 1995, 130 (01) :207-215

[10]

Chen YG, 2006, EXP BIOL MED, V231, P534

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