Promoters tissue plasminogen activator

Loscalzo J, Vaughan DE. Tissue plasminogen activator promotes platelet disaggregation in plasma. J Clin Invest. 1987 79 1749-1755. 

The mechanisms of the influence of the SNS on the induction of CD8+ Tregs are likely directed towards both the activation and function of these cells (fig. 2). Sympathetic neurons are a source of (i) norepinephrine that has strong immunoregulatory effects [35] including the proliferation of liver NKT cells necessary for the initiation of contact sensitivity reactions (ii) immunomodulatory NPY [38] that may promote the production of IFN-y necessary for the function of CD8+ suppressor T cells (see below), and (hi) tissue plasminogen activator (t-PA) [41] that converts plasminogen to plasmin that in turn is an activator of immunosuppressive TGF-(3 [42]. 

Protein C. This vitamin K-dependent glycoprotein serine protease zymogen is produced in the liver. It is an anticoagulant with species specificity (19—21). Protein C is activated to Protein Ca by thrombomodulin, a protein that resides on the surface of endothelial cells, plus thrombin in the presence of calcium. In its active form, Protein Ca selectively inactivates, by proteolytic degradation, Factors V, Va, VIII, and Villa. In this reaction the efficiency of Protein Ca is enhanced by complex formation with free Protein S. In addition, Protein Ca activates tissue plasminogen activator, which promotes the conversion of plasminogen [9001-91-6] to plasmin [9001-90-5]. 

The first successful therapeutic protein made in a transgenic system was human tissue plasminogen activator regulated by a milk-directed promoter for accumulation in mouse milk [5]. Human growth hormone, which was one of the first proteins produced using recombinant microbial systems in the early 1980s, became the first human protein expressed in plants (tobacco cells) in 1986 [6]. Since then, over 200 biotherapeutics of diverse origin. 

Tissue plasminogen activator Promotes the dissolving of blood clots... 

If the patient received tissue plasminogen activator, give I.V. heparin to promote patency in the affected coronary artery. 

Fig. 3 Pathogenesis of acute vascular rejection. Activation of endothelium by xenoreactive antibodies (Ab), complement (C), platelets, and perhaps by inflammatory cells (natural killer (NK) cells and macrophages (M0) leads to the expression of new pathophysiologic properties. These new properties, such as the synthesis of tissue factor (TF) and plasminogen activator inhibitortype 1 (PAI-1), promote coagulation the synthesis of E-selectin and cytokines such as I LI a promote inflammation. These changes in turn cause thrombosis, ischemia, and endothelial injury, the hallmarks of acute vascular rejection. (Adapted from Nature 1998 392(Suppl.) 11-17, with permission.) (See Color Plate p. xxiii).

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