scholarly journals Effect of Obesity on Tissue Factor, Tissue Plasminogen Activator and Plasminogen Activator Inhibitor Among Obese People in Sapele Southern Nigeria

2021 ◽  
Vol 7 (3) ◽  
pp. 81
Author(s):  
Kingsley Chukwuka Amaihunwa ◽  
Emmanuel Asuquo Etim ◽  
Everista Odaburhine Osime ◽  
Zacchaeus Awortu Jeremiah
1993 ◽  
Vol 69 (03) ◽  
pp. 253-258 ◽  
Author(s):  
Robert A Bok ◽  
Harry S Jacob ◽  
Jozsef Balla ◽  
Margaret Juckett ◽  
Theresa Stelle ◽  
...  

SummaryHerpes simplex virus (HSV) infection is histopathologically associated with vascular injury, fibrinoid necrosis and inflammatory cell infiltrates. We have previously shown in vitro that HSV infection of human umbilical vein endothelial cells (HUVEC) promotes a procoagulant phenotype manifest by the induction of tissue factor, the loss of thrombomodulin, and an increase in platelet adhesion. In these studies we examined the effects of HSV infection on HUVEC plasminogen activator inhibitor type 1 (PAI-1) and tissue plasminogen activator (t-PA). HSV infection caused the loss of PAI-1 in the extracellular matrix (ECM) and that released into the supernatant of HUVEC. Both activity and antigen levels of the Serpin inhibitor are diminished as a result of HSV infection. The loss of inhibitor is not secondary to diminished vitronectin (Vn), the primary binding protein of PAI-1 in the ECM, but appears to be secondary to decreased synthesis at the RNA level. Tissue plasminogen activator (t-PA). synthesis is also decreased in endothelial HSV infection. PAI-1 loss may further promote a procoagulant phenotype in HSV infection in vivo.


1990 ◽  
Vol 265 (1) ◽  
pp. 109-113 ◽  
Author(s):  
T L Lindahl ◽  
P I Ohlsson ◽  
B Wiman

The structural events taking place during the reaction between PAI-1 (plasminogen-activator inhibitor 1) and the plasminogen activators sc-tPA (single-chain tissue plasminogen activator) and tc-tPA (two-chain tissue plasminogen activator) were studied. Complexes were formed by mixing sc-tPA or tc-tPA with PAI-1 in slight excess (on an activity basis). The complexes were purified from excess PAI-1 by affinity chromatography on fibrin-Sepharose. Examination of the purified complexes by SDS/polyacrylamide-gel electrophoresis (SDS/PAGE) and N-terminal amino acid sequence analysis demonstrated that a stoichiometric 1:1 complex is formed between PAI-1 and both forms of tPA. Data obtained from both complexes revealed the amino acid sequences of the parent molecules and, in addition, a new sequence: Met-Ala-Pro-Glu-Glu-. This sequence is found in the C-terminal portion of the intact PAI-1 molecule and thus locates the reactive centre of PAI-1 to Arg346-Met347. The proteolytic activity of sc-tPA is demonstrated by its capacity to cleave the ‘bait’ peptide bond in PAI-1. The complexes were inactive and dissociated slowly at physiological pH and ionic strength, but rapidly in aq. NH3 (0.1 mol/l). Amidolytic tPA activity was generated on dissociation of the complexes, corresponding to 0.4 mol of tPA/mol of complex. SDS/PAGE of the dissociated complexes indicated a small decrease in the molecular mass of PAI-1, in agreement with proteolytic cleavage of the ‘bait’ peptide bond during complex-formation.


1987 ◽  
Author(s):  
J Petäjä ◽  
G Myllylä ◽  
V Rasi ◽  
E Vahtera

We have studied the fibrinolytic system in one asymptomatic and six symptomatic members of a family with recurrent DVTs in three generations. Tissue plasminogen activator activity (TPA) and fast acting inhibitor of TPA (PAI) were determined using chromogenic substrate and TPA antigen with ELISA. Measurements were made at rest and after 10 and 20 minutes of venous occlusion (VO). 17 healthy subjects served as controls. The mean TPA in the seven family members was significantly lower than in controls at 10 and 20 min VO (p< 0.01).TPA was below the lowest value of controls (<1.7 U/ml) in five of the six patients with DVT at 10 min VO and remained below the range of controls in three at 20 min VO (<3.3 U/ml). The lowered TPA activity was associated with impaired release of TPA antigen (mean level at 10 min VO 12.A ng/ml, controls 19.5 ng/ml, p<0.05; at 20 min VO 18.2 ng/ml, controls 43.2 ng/ml, p<0.01). Four .patients with and one without DVT had TPA antigen below the lowest level of controls at 10 and/or 20 min VO. The level of'PAI at rest was normal in all cases (from 0.6 to 1.7 U/ml, controls from 0 to 3.7 U/ml). In accordance with low release of TPA antigen PAI was consumed less during VO in patients than in controls (mean level at 20 min VO 0.9 U/ml, controls 0.4 U/ml, p<0.05). The levels of antithrombin III, protein C, protein S, plasminogen, fibrinogen, F V, F VIII:C, vWf:Ag, fibrinopeptide A and beta-thromboglobulin were normal . Circulating anticoagulant was not found. It is concluded that impaired release of TPA, independent of PAI, is associated with DVT in this family. The pattern of inheritance suggested autosomal dominant trait.


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