WHAT HAVE MAST-CELLS TO DO WITH EDEMA FORMATION, THE CONSECUTIVE REPAIR AND FIBRINOLYSIS

Mast cells (MC) have been implicated in the activation of vascular end othelial cells, capillary leak formation, transmigration of white bloo d cells, and translocation of fibrinogen (and other plasma molecules) into the tissues, with consecutive edema formation. However, the mecha nisms of repair that lead to tissue reconstitution after MC activation and edema formation have not been defined so far. In the present arti cle, the possible contribution of MC to repair, in particular fibrinol ysis, is discussed. Thus, accumulating evidence exists that human MC e xpress and release the tissue-type plasminogen activator (tPA) in a co nstitutive manner. MC also express the urokinase receptor (uPAR) and h eparin. Most importantly, however, MC lack plasminogen activator inhib itors (PAI-1, PAI-2, PAI-3). In line with this 'pro-fibrinolytic' prof ile of antigens, MC supernatants induce plasminogen-to-plasmin convers ion and fibrin clot lysis in vitro. The c-kit ligand SCF upregulates u PAR expression, and the release of tPA from MC. These observations poi nt to an important role of MC in endogenous fibrinolysis, a hitherto u nrecognized (repair) function of this cell.