Literature DB >> 3264718

Plasminogen activator inhibitor (PAI-1) in plasma and platelets.

N A Booth1, A J Simpson, A Croll, B Bennett, I R MacGregor.   

Abstract

The distribution of PAI-1 in the plasma and platelets of normal individuals and of patients with platelet abnormalities was studied. An ELISA, capable of measuring PAI-1 in plasma at 1.5 ng/ml, and a functional assay of t-PA inhibition were used to assay platelet-free plasma (PFP), platelet-rich plasma in which the platelets were lysed (PRP) and serum. The PAI-1 concentration of normal PFP was 21.0 +/- 7.2 ng/ml (mean +/- SD) and those of PRP and serum were 282.6 +/- 68.0 and 270.3 +/- 71.9 ng/ml. The concentration of PAI-1 in PRP was proportional to the platelet count with 0.67 +/- 0.18 ng/10(6) platelets. Patients with thrombocytopenia had approximately normal PAI-1 concentrations in PFP; the extremely low concentrations in serum or PRP reflected the platelet count. A patient with grey platelet syndrome showed a comparable pattern, confirming that PAI-1 occurs in the platelet alpha-granules and indicating that the plasma concentration of PAI-1 is independent of the platelet pool of PAI-1. The median inhibitory activities towards t-PA were 1.6, 8.7 and 8.3 units/ml in normal PFP, PRP and serum respectively. PAI-1 in PFP had a median specific activity (units/mg PAI-1) about 5-fold higher than platelet PAI-1. Plasma and platelets represent two distinct pools of PAI-1, both of which should be considered in studies on the relationship between circulating PAI-1 and thrombotic disease.

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Year:  1988        PMID: 3264718     DOI: 10.1111/j.1365-2141.1988.tb02490.x

Source DB:  PubMed          Journal:  Br J Haematol        ISSN: 0007-1048            Impact factor:   6.998


  57 in total

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8.  Polyphosphate colocalizes with factor XII on platelet-bound fibrin and augments its plasminogen activator activity.

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9.  Increased 18F-FDG uptake is predictive of rupture in a novel rat abdominal aortic aneurysm rupture model.

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10.  Tissue plasminogen activator, plasminogen activator inhibitors, and activator-inhibitor complex in liver disease.

Authors:  K Leiper; A Croll; N A Booth; N R Moore; T Sinclair; B Bennett
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