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Plasminogen activators and inhibitors in peritoneal tissue
Author(s) -
HOLMDAHL LENA,
FALKENBERG MÅRTEN,
IVARSSON MARIELOUISE,
RISBERG BO
Publication year - 1997
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1997.tb00535.x
Subject(s) - mesothelium , fibrin , inflammation , fibrinolysis , plasminogen activator , tissue plasminogen activator , pathology , t plasminogen activator , plasmin , plasminogen activator inhibitor 1 , wound healing , chemistry , peritoneum , medicine , immunology , endocrinology , biochemistry , enzyme
Serosal trauma elicits an inflammatory response which leads to the deposition of fibrin at injured sites, the residuals of which appear to be essential in excessive tissue repair and formation of intraabdominal adhesions. Local plasminogen activity may modulate this early phase of tissue repair. The present study was undertaken to investigate the distribution and cellular expression of plasminogen activators and their inhibitors in human peritoneal normal and inflamed tissue. Tissue‐type plasminogen activator (t‐PA) was expressed in subserosal capillary walls, and in normal mesothelium, but not in inflammation. Immunoreactivity for the plasminogen activator inhibitor type 1 (PAI‐1) was present in normal mesothelium, and substantially increased in inflammation, where, in addition, immunoreactivity was found throughout the submesothelial tissue. This PAI‐1 was partly co‐localized with macrophages, as was the urokinase plasminogen activator (u‐PA), suggesting an involvement of these cells in peritoneal tissue fibrinolysis. Inflammation or abrasion of the mesothelium during surgery is likely to cause a depletion of the local t‐PA source and expose the potentially PAI‐1‐containing submesothelial tissue, thus promoting persistence of fibrin and formation of adhesions.