Amino Acid Sequence and Inhibitory Activity of Rhesus Monkey Tissue Factor Pathway Inhibitor (TFPI): Comparison with Human TFPI1

Kamei, Satoshi; Kamikubo, Yu-ichi; Hamuro, Tsutomu; Fujimoto, Hidehiro; Ishihara, Minako; Yonemura, Hiroshi; Miyamoto, Seiji; Funatsu, Asami; Enjyoji, Keiichi; Abumiya, Takeo; Miyata, Toshiyuki; Kato, Harubumi

doi:10.1093/oxfordjournals.jbchem.a124400

Cited by 34 publications

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“…In an earlier experiment we cloned monkey TFPI cDNA, determined the amino acid sequence of monkey TFPI, and prepared recombinant monkey TFPI (rTFPI) and its polyclonal and monoclonal antibodies. 12 In the present study we demonstrate that LDL/VLDL-associated TFPI is increased in crab-eating monkeys fed a high-cholesterol diet. We also discuss the changes in TFPI levels after injection of heparin into these monkeys.…”

Section: Response Of Plasma Tissue Factor Pathway Inhibitor To Diet-isupporting

confidence: 56%

“…Human factor X, 13 human factor VII, 14 monkey rTFPI, and mouse anti-monkey rTFPI monoclonal antibody 12 were prepared as described. Factor VII was activated into factor Vila by factor Xa.…”

Section: Methods Materialsmentioning

confidence: 99%

“…Blood collection was performed before (-10 and 0 weeks) and after (4,12,16, and 20 weeks) the animals began the high-cholesterol diet. The mean plasma cholesterol level of six monkeys before initiation of the high-cholesterol diet was 4.57±0.67 mmol/L.…”

Section: Cholesterol and Tfpi Activity Levels In Plasmamentioning

confidence: 99%

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Response of plasma tissue factor pathway inhibitor to diet-induced hypercholesterolemia in crab-eating monkeys.

Abumiya

Nakamura

Takenaka

et al. 1994

Arterioscler Thromb

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Tissue factor pathway inhibitor (TFPI), a protease inhibitor associated with lipoproteins in plasma and endothelial cells, can inhibit the initial reactions of the tissue factor-mediated coagulation pathway. A positive relationship between TFPI and cholesterol has been demonstrated in human plasma. To investigate this relation in more detail, in the present study we measured TFPI in the plasma of monkeys on a high-cholesterol diet. After diet treatment, cholesterol levels and TFPI activity were increased 3-and 1.5-fold, respectively. Three forms of TFPI, low-density lipoprotein (LDL)/very-low-density lipoprotein (VLDL)-associated TFPI, high-density lipoprotein (HDL)-associated TFPI, and free TFPI, were measured after gel filtration of plasma. In hypercholesterolemic monkeys, levels of TFPI activity and T he extrinsic blood coagulation pathway is triggered by the interaction between tissue factor (TF) and factor VII, which leads to activation of the precursors of the serine proteases, factor VII, factor IX, factor X, and prothrombin, resulting in the generation of thrombin. (For a review see References 1 and 2.) These reactions are regulated by several different mechanisms, eg, inactivation of cofactors by activated protein C and inactivation of activated proteases by protease inhibitors such as antithrombin III. TF pathway inhibitor (TFPI), a protease inhibitor with three tandem Kunitz-type inhibitory domains, inhibits factor Vila and factor Xa in the presence of TF, so that TFPI is an inhibitor of the initial reaction of the extrinsic pathway. (For reviews see References 3 through 7.)The most striking characteristics of TFPI are its association with lipoproteins in plasma and endothelial cells. It has been demonstrated that three forms of TFPI, low-density lipoprotein (LDL)/very-low-density lipoprotein (VLDL)-associated TFPI, high-density lipoprotein (HDL)-associated TFPI, and the free form of TFPI, can be detected by gel filtration of human plasma; it has also been shown that heparin infusion markedly increases the free form of TFPI, which is thought to be derived from

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Section: Response Of Plasma Tissue Factor Pathway Inhibitor To Diet-isupporting

confidence: 56%

Section: Methods Materialsmentioning

confidence: 99%

See 1 more Smart Citation

Response of plasma tissue factor pathway inhibitor to diet-induced hypercholesterolemia in crab-eating monkeys.

Abumiya

Nakamura

Takenaka

et al. 1994

Arterioscler Thromb

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“…23 Plasma thrombomodulin concentration was measured by an ELISA kit (a gift from Asahi Chemical Industry) based on a sandwich ELISA with two monoclonal antibodies recognizing different epitopes of thrombomodulin. 24 …”

Section: Determination Of Plasma Tfpi Concentrationmentioning

confidence: 99%

Deranged Blood Coagulation Equilibrium As A Factor of Massive Liver Necrosis Following Endotoxin Administration in Partially Hepatectomized Rats

et al. 1999

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Activated Kupffer cells provoke massive liver necrosis after endotoxin stimulation through microcirculatory disturbance caused by sinusoidal fibrin deposition in rats undergoing 70% hepatectomy. In these rats, serum activities of purine nucleoside phosphorylase (PNP) and alanine transaminase (ALT) were increased at 1 and 5 hours, respectively, following endotoxin administration. When 70% resected liver was perfused with Dulbecco's modified Eagle medium (DMEM) containing heat-inactivated fetal calf serum, the increase in both enzyme activities was not affected by addition of endotoxin during perfusion, suggesting that activated Kupffer cells injured neither sinusoidal endothelial cells nor hepatocytes. The activity of tissue factor, an initiator of blood coagulation cascade, was much higher in Kupffer cells isolated from partially hepatectomized rats than in those from normal rats. In contrast, mRNA expressions of tissue factor pathway inhibitor (TFPI) as well as thrombomodulin were almost undetectable in normal and partially resected livers. 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. In these rats, endotoxin-induced liver injury was significantly attenuated compared with rats given no TFPI. Similar attenuation was also found in rats receiving recombinant human thrombomodulin. 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 Massive liver necrosis develops after endotoxin administration in rats pretreated with heat-killed Propionibacterium acnes or those undergoing 70% liver resection as a result of microcirculatory disturbance caused by sinusoidal fibrin deposition. [1][2][3] In both models, Kupffer cells and hepatic macrophages are activated to provoke endothelial cell injury and fibrin deposition in the hepatic sinusoids. 2-6 However, an apparent difference exists in the stimulatory state of Kupffer cells and hepatic macrophages between both models, because activated Kupffer cells in the partial-hepatectomy model produced fewer cytotoxic mediators such as superoxide anions and tumor necrosis factor ␣ in response to endotoxin administration compared with activated hepatic macrophages in the P. acnes model, 6,7 although both cells can release a large amount of superoxide anions after stimulation with phorbol 12-myristate 13-acetate. 3,4 Northern blot analysis revealed that such difference resulted from expression of endotoxin receptors on the cells; P. acnes-treated rat liver showed increased mRNA expression of CD14, a receptor for lipopolysaccharide and its binding protein complex, compared with normal liver, while such expression was markedly reduced in partially hepatectomized rat liver. 7 In the P. acnes model, activated hepatic macrophages after endotoxin stimulatio...

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“…Total-TFPI antigen levels were measured by a onestep sandwich ELISA kit (Chemo-Sero-Therapeutic Research Institute) with polyclonal antibody and monoclonal antibody [15]. The rabbit anti-TFPI polyclonal antibody was immobilized to the solid phase (microplate well), and the monoclonal antibody, which conjugated with HRP, recognized the specific conformation formed between the K1 and K2 domains.…”

Section: Methodsmentioning

confidence: 99%

Increased tissue factor pathway inhibitor in patients with acute myocardial infarction

et al. 1997

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We examined hemostatic abnormalities in 23 patients with acute myocardial infarction (AMI), 10 with pulmonary embolism (PE), and 10 with deep vein thrombosis (DVT). At the onset of AMI, plasma levels of tissue-type plasminogen activator (t-PA), PA inhibitor-I (PAI-I), fibrin-D-dimer, thrombin-antithrombin complex (TAT), and plasmin-plasmin inhibitor complex (PPIC) were significantly increased. Both the plasma total TFPI and free-TFPI levels in the AMI patients were significantly higher than those in the healthy volunteers, PE patients, and DVT patients. There was no significant difference in total TFPI or free-TFPI among patients with PE, those with DVT, and healthy volunteers. One hour after percutaneous transluminal coronary angioplasty (PTCA) in the AMI group, the total TFPI level was further increased, and it was significantly reduced 24 hr after PTCA, to a level similar to that in healthy volunteers. Free-TFPI showed a pattern similar to that of total TFPI. The ratio of free-TFPI/total TFPI was highest 1 hr after PTCA. Increased TFPI in AMI patients might be released from ischemic tissues. Am.

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Amino Acid Sequence and Inhibitory Activity of Rhesus Monkey Tissue Factor Pathway Inhibitor (TFPI): Comparison with Human TFPI1

Cited by 34 publications

References 0 publications

Response of plasma tissue factor pathway inhibitor to diet-induced hypercholesterolemia in crab-eating monkeys.

Response of plasma tissue factor pathway inhibitor to diet-induced hypercholesterolemia in crab-eating monkeys.

Deranged Blood Coagulation Equilibrium As A Factor of Massive Liver Necrosis Following Endotoxin Administration in Partially Hepatectomized Rats

Increased tissue factor pathway inhibitor in patients with acute myocardial infarction

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