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Titolo:
WHAT HAVE MAST-CELLS TO DO WITH EDEMA FORMATION, THE CONSECUTIVE REPAIR AND FIBRINOLYSIS
Autore:
VALENT P; SILLABER C; BAGHESTANIAN M; BANKL HC; KIENER HP; LECHNER K; BINDER BR;
Indirizzi:
UNIV VIENNA,DEPT INTERNAL MED 1,DIV HEMATOL & & HEMOSTASEOL,WAHRINGERGURTEL 18-20 A-1090 VIENNA AUSTRIA UNIV VIENNA,INST PHYSIOL A-1090 VIENNA AUSTRIA UNIV VIENNA,INST CLIN PATHOL A-1090 VIENNA AUSTRIA UNIV VIENNA,DEPT INTERNAL MED 3,DIV RHEUMATOL A-1090 VIENNA AUSTRIA
Titolo Testata:
International archives of allergy and immunology
fascicolo: 1, volume: 115, anno: 1998,
pagine: 2 - 8
SICI:
1018-2438(1998)115:1<2:WHMTDW>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
IMMEDIATE HYPERSENSITIVITY REACTIONS; TUMOR-NECROSIS-FACTOR; PLASMINOGEN-ACTIVATOR; LEUKOCYTE ADHESION; MOUSE SKIN; KIT-LIGAND; C-KIT; MICE; TRYPTASE; RELEASE;
Keywords:
MAST CELLS; FIBRINOLYSIS; REPAIR; TISSUE-TYPE PLASMINOGEN ACTIVATOR; PLASMINOGEN ACTIVATOR INHIBITOR; C-KIT; STEM CELL FACTOR; HEPARIN;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
50
Recensione:
Indirizzi per estratti:
Citazione:
P. Valent et al., "WHAT HAVE MAST-CELLS TO DO WITH EDEMA FORMATION, THE CONSECUTIVE REPAIR AND FIBRINOLYSIS", International archives of allergy and immunology, 115(1), 1998, pp. 2-8

Abstract

Mast cells (MC) have been implicated in the activation of vascular endothelial cells, capillary leak formation, transmigration of white blood cells, and translocation of fibrinogen (and other plasma molecules)into the tissues, with consecutive edema formation. However, the mechanisms of repair that lead to tissue reconstitution after MC activation and edema formation have not been defined so far. In the present article, the possible contribution of MC to repair, in particular fibrinolysis, is discussed. Thus, accumulating evidence exists that human MC express and release the tissue-type plasminogen activator (tPA) in a constitutive manner. MC also express the urokinase receptor (uPAR) and heparin. Most importantly, however, MC lack plasminogen activator inhibitors (PAI-1, PAI-2, PAI-3). In line with this 'pro-fibrinolytic' profile of antigens, MC supernatants induce plasminogen-to-plasmin conversion and fibrin clot lysis in vitro. The c-kit ligand SCF upregulates uPAR expression, and the release of tPA from MC. These observations point to an important role of MC in endogenous fibrinolysis, a hitherto unrecognized (repair) function of this cell.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/09/20 alle ore 02:07:32