The phospholipid requirement of tissue factor in blood coagulation

Nemerson, Yale

doi:10.1172/jci105716

Cited by 143 publications

(63 citation statements)

References 31 publications

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“…These patients appeared to have dif- Glomerular PCA was inhibited by concanavalin A, and the specific nature of this inhibition was confirmed by the ability of the conjugate sugar a-methyl-mannoside to block this effect. This is also consistent with tissue factor, a membrane bound glycoprotein (19) that is functionally inhibited when bound to concanavalin A (36,37).…”

Section: Discussionsupporting

confidence: 77%

Glomerular procoagulant activity in human proliferative glomerulonephritis.

Tipping¹,

Dowling²,

Holdsworth³

1988

J. Clin. Invest.

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Mechanisms for initiation of glomerular fibrin deposition were studied using renal tissue obtained from two patients with rapidly progressive, crescentic glomerulonephritis. Histological examination showed extensive glomerular monocyte infiltration and fibrin deposition in both patients. Sonicated cell suspensions of isolated glomeruli from these patients contained markedly augmented levels of procoagulant activity (PCA) compared with the levels found in normal glomeruli. This PCA was characterized as tissue factor by its functional dependence on Factors VII and V, independence of Factors VIII and XII, inhibition by concanavalin A and phospholipase C, and association with cell membranes. Its coagulant activity was also inhibited by a specific monoclonal anti-human tissue factor antibody. Tissue factor could be identified in glomeruli from these two patients by indirect immunofluorescence using this antibody. These studies implicate extrinsic pathway activation via tissue factor in intraglomerular deposition of fibrin in these patients. Activated monocytes, known to be a potent source of procoagulant activity and seen in large numbers within glomeruli from these patients, are a likely source of this tissue factor.

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Section: Discussionsupporting

confidence: 77%

Glomerular procoagulant activity in human proliferative glomerulonephritis.

Tipping¹,

Dowling²,

Holdsworth³

1988

J. Clin. Invest.

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“…Control and balloon-injured rat aortic media and adventitia were separately immersed in TBS and then sonicated at 20 kHz for 20 s (model W375; Heat Systems-Ultrasonics Inc., Farmingdale, NY). 50-Ml aliquots were assayed in duplicate for TF activity using modifications ofa standard two-stage procedure (28,29). Each aliquot was incubated at 37°C for 1 min with 50 ,ul of rat Factor VII-X concentrate and 50 ,u ofa 5-mM CaCl2, 12.5-MM phosphatidyl serine/phosphatidyl choline (30/70; wt/wt) in TBS.…”

Section: Methodsmentioning

confidence: 99%

Tissue factor is rapidly induced in arterial smooth muscle after balloon injury.

Marmur¹,

Rossikhina²,

Guha³

et al. 1993

J. Clin. Invest.

227

117

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Tissue factor (TF) is a major activator of the coagulation cascade and may play a role in initiating thrombosis after intravascular injury. To investigate whether medial vascular smooth muscle provides a source of TF following arterial injury, the induction of TF mRNA and protein was studied in balloon-injured rat aorta. After full length aortic injury, aortas were harvested at various times and the media and adventitia separated using collagenase digestion and microscopic dissection. In uninjured aortic media, TF mRNA was undetectable by RNA blot hybridization. 2 h after balloon injury TF mRNA levels increased markedly. Return to near baseline levels occurred at 24 h. In situ hybridization with a 35S-labeled antisense rat TF cRNA probe detected TF mRNA in the adventitia but not in the media or endothelium of uninjured aorta. 2 h after balloon dilatation, a marked induction of TF mRNA was observed in the adventitia and media. Using a functional clotting assay, TF procoagulant activity was detected at low levels in uninjured rat aortic media and rose by 10-fold 2 h after balloon dilatation.Return to baseline occurred within 4 d. These data demonstrate that vascular injury rapidly induces active TF in arterial smooth muscle, providing a procoagulant that may result in thrombus initiation or propagation. (J. Clin. Invest. 1993.

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“…A more specific assay for tissue thromboplastin thani the one-stage test with normal plasma was performed (20,21). 0.1 ml of the resuspended leukocyte incubate wvas added to 0.1 ml of a bariu-m sulfate eluate of normal hum-an serum.…”

Section: Methodsmentioning

confidence: 99%