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Thrombin signal transduction of the fibrinolytic system in human adult venous endothelium in vitro.

Artikel i vetenskaplig tidskrift
Författare H E Rydholm
Peter Falk
Elsa M Eriksson
Bo Risberg
Publicerad i Scandinavian journal of clinical and laboratory investigation
Volym 58
Nummer/häfte 4
Sidor 347-52
ISSN 0036-5513
Publiceringsår 1998
Publicerad vid Institutionen för de kirurgiska disciplinerna
Institutionen för de kirurgiska disciplinerna, Avdelningen för anestesiologi och intensivvård
Institutionen för de kirurgiska disciplinerna, Avdelningen för kirurgi
Sidor 347-52
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Adult, Cells, Cultured, Endothelium, Vascular, cytology, metabolism, Fibrinolysis, GTP-Binding Proteins, physiology, Genistein, pharmacology, Humans, Plasminogen Activator Inhibitor 1, biosynthesis, Signal Transduction, Thrombin, pharmacology, Tissue Plasminogen Activator, biosynthesis
Ämneskategorier Kirurgi, Cell- och molekylärbiologi

Sammanfattning

Thrombin can regulate the-fibrinolytic system by increasing the endothelial production of both tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type-1 (PAI-1). The thrombin receptor transducts signals through the GTP-binding protein system, the classical pathway being the Galpha q-protein. The purpose of the present study was to examine the roles of Galpha i-protein and tyrosine kinases in the thrombin signal transduction of t-PA and PAI-1 production from human adult vein endothelial cells (HAVEC). t-PA and PAI-1 antigen were analysed in conditioned medium from cultured HAVEC after 16 h incubation. Data are expressed as percentages of basal release (100%), means +/- 95% confidence intervals. Thrombin increased t-PA and PAI-1 production (234 +/- 42% and 211 +/- 42%, respectively). Pertussis toxin (PTX) (inhibiting Galpha i-pathway) reduced basal PAI-1 (66 +/- 8%), but had only a weak influence on basal t-PA production. Pertussis toxin and genistein (inhibiting tyrosine kinase) significantly reduced the thrombin induction of both t-PA and PAI-1 (PTX: 142 +/- 23% and 146 +/- 19%, respectively, genistein: 156 +/- 42% and 76 +/- 24%, respectively). The present study demonstrated that thrombin can increase the production of t-PA and PAI-1 by transducting signals through the Galpha i and tyrosine kinase pathway, in addition to the Galpha q/protein kinase C pathway as has been found previously.

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