Disease relevance of Tfpi

• Intratracheal gene transfer of tissue factor pathway inhibitor attenuates pulmonary fibrosis [1].
• Intratracheal administration of an adenovirus vector expressing TFPI significantly decreased bleomycin-induced procoagulant and thrombin generation resulting in a strong inhibition of pulmonary fibrosis [1].
• Effects of recombinant human tissue factor pathway inhibitor on thrombus formation and its in vivo distribution in a rat DIC model [2].
• Expression of tissue factor and tissue factor pathway inhibitor in rats lungs with lipopolysaccharide-induced disseminated intravascular coagulation [3].
• The TFPI expression in cardiomyocytes was confirmed by Northern blotting with rat cardiomyocytes and also by immunostaining with anti-TFPI antibody on human heart specimens from patients either with sarcoidosis, myocarditis or myocardial infarction [4].

High impact information on Tfpi

• The carboxy terminus of tissue factor pathway inhibitor is required for interacting with hepatoma cells in vitro and in vivo [5].
• Maximal induction of interleukin 6 mRNA required a brief, 30-min stimulation with factor Xa, unaffected by subsequent addition of tissue factor pathway inhibitor [6].
• The low density lipoprotein receptor-related protein mediates the cellular degradation of tissue factor pathway inhibitor [7].
• These results suggest that fibrin deposition developing in 70% hepatectomized rats after endotoxin administration may be caused by deranged blood coagulation in the hepatic sinusoids through increasing tissue factor activity in Kupffer cells and minimal TFPI and thrombomodulin in endothelial cells [8].
• When recombinant human TFPI was injected intravenously in 70% hepatectomized rats, TFPI was markedly stained on the surfaces of sinusoidal endothelial cells and microvilli of hepatocytes on immunohistochemistry [8].

Chemical compound and disease context of Tfpi

• The imbalance between TF and TFPI seems to be important in promoting fibrin thrombus formation in the lung of endotoxin induced DIC condition [9].

Biological context of Tfpi

• The expression of tissue factor and tissue factor pathway inhibitor in aortic smooth muscle cells is up-regulated in synthetic compared to contractile phenotype [10].
• CONCLUSIONS: Rapid atrial pacing acutely downregulated the gene expression of TM and TFPI in the atrial endocardium, thereby inducing local coagulation imbalance on the internal surface of the atrial cavity [11].
• Rapid atrial pacing for 8 hours significantly decreased TM and TFPI mRNA levels in the left atrium but not in the ventricle, leading to the downregulation of their immunoreactive proteins [11].
• Production of tissue factor pathway inhibitor in cardiomyocytes and its upregulation by interleukin-1 [4].
• We isolated cDNA for rat TFPI by screening a lambda gt10 rat liver cDNA library [12].

Anatomical context of Tfpi

• Tissue factor (TF) and its specific inhibitor TF pathway inhibitor (TFPI) are produced by vascular smooth muscle cells (SMCs) in vitro and are increased in vivo in atherosclerotic compared to normal vessels [10].
• Thrombomodulin and tissue factor pathway inhibitor in endocardium of rapidly paced rat atria [11].
• On Northern blot analysis of rat TFPI mRNA, rat TFPI mRNA was detected as two forms with different molecular sizes, 4.0 and 1.4 kb, which were expressed abundantly in heart, lung, kidney, and aortic endothelial cells [12].
• Furthermore, tissue factor pathway inhibitor, a natural anticoagulant for the extrinsic pathway of the coagulation system, also attenuates LPS-induced inflammatory responses in rats by inhibiting TNF-alpha production by monocytes [13].
• Exogenous TFPI was mainly identified in Kupffer cells, macrophages, and on the microvascular endothelial lining of different organs [2].

Associations of Tfpi with chemical compounds

• None of the used angiotensin metabolites altered TFPI or TPA mRNA expression levels [14].
• Ang II increased PAI-1 and TF mRNA expression without affecting that of TPA or TFPI [15].
• Asn-linked oligosaccharides terminating with the sequence SO4-4GalNAc beta 1,4GlcNAc beta 1,2Man alpha (S4GGnM) are present on the glycoprotein hormones lutropin and thyrotropin, pro-opiomelanocortin, and tissue factor pathway inhibitor [16].
• Experimental haemorrhagic effect of two-domain non-glycosylated tissue factor pathway inhibitor compared to low molecular weight heparin [17].
• While there was no significant difference in AT-III, TFPI and protein C activities between SHR-SP and WKY rats, C1 inhibitor activity was significantly higher in SHR-SP than in WKY rats [18].

Regulatory relationships of Tfpi

• TFPI is a multivalent Kunitz-type protease inhibitor that inhibits factor Xa via its second Kunitz domain and the factor VIIa/tissue factor (TF) complex via its first Kunitz domain [19].

Other interactions of Tfpi

• Angiotensin II increases plasminogen activator inhibitor-1 and tissue factor mRNA expression without changing that of tissue type plasminogen activator or tissue factor pathway inhibitor in cultured rat aortic endothelial cells [15].
• Human ryudocan from endothelium-like cells binds basic fibroblast growth factor, midkine, and tissue factor pathway inhibitor [20].

Analytical, diagnostic and therapeutic context of Tfpi

• The intimal thickening that follows vascular injury is inhibited by periprocedural tissue factor pathway inhibitor (TFPI) treatment in animal models [19].
• The effect of tissue factor pathway inhibitor on hepatic ischemic reperfusion injury of the rat [21].
• Although TF was strongly stained on endothelial cells and Kupffer cells accumulating to the site of the necrosis in the control group, the area of the necrosis and the grade of TF staining were significantly reduced in the TFPI-treated group [21].

References