Tryptase from rat mast cells converts bovine prothrombin to thrombin

Kido, Hiroshi; Fukusen, Naomi; Katunuma, Nobuhiko; Morita, Takashi; Iwanaga, Sadaaki

doi:10.1016/0006-291x(85)91177-5

Cited by 30 publications

(12 citation statements)

References 18 publications

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“…38 Conversely, mast cells are able to convert prothrombin to thrombin by the release of tryptase. 39 Interestingly, it has been shown that in C1-inhibitor deficiency, both hereditary and acquired, acute attacks are associated with the generation of thrombin. 25 Further, heparin has been shown to inhibit the whealand-flare reaction on ASST 10,22 ; heparin is an activator of antithrombin-III, a plasma protein that binds irreversibly to some serine protease enzymes (factors XIa, IXa, Xa, VIIa, and thrombin) and blocks their activity.…”

Section: Discussionmentioning

confidence: 99%

Plasma of patients with chronic urticaria shows signs of thrombin generation, and its intradermal injection causes wheal-and-flare reactions much more frequently than autologous serum

Asero¹,

Tedeschi

Riboldi

et al. 2006

Journal of Allergy and Clinical Immunology

196

210

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Section: Discussionmentioning

confidence: 99%

Plasma of patients with chronic urticaria shows signs of thrombin generation, and its intradermal injection causes wheal-and-flare reactions much more frequently than autologous serum

Asero¹,

Tedeschi

Riboldi

et al. 2006

Journal of Allergy and Clinical Immunology

196

210

View full text Add to dashboard Cite

“…Recently, we have been luckier when, based on the observation of a higher prevalence of positive autologous plasma skin test over autologous serum skin test, we started looking at the coagulation cascade and were able to demonstrate that CU is characterized by thrombin generation,[29] which is the result of an activation of the tissue pathway of blood coagulation [30,31]. Notably, studies in animal models have shown that thrombin is able to induce mastcell degranulation,[32] and in rat mast cell populations, the response to thrombin is equipotent with Fc ε RI-mediated activation [33]. Thus (although evidence that thrombin induces mast cells degranulation in humans is still missing), thrombin might be a candidate mast-cell activating factor, at least in patients whose sera don't contain autoantibodies and show an activation of coagulation cascade.…”

Section: Who Activates Mast Cells When Autoantibodies Are Not Present?mentioning

confidence: 99%

Eosinophils in Chronic Urticaria: Supporting or Leading Actors?

Asero

Cugno

Tedeschi

2009

World Allergy Organization Journal

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Although their number may be increased in skin lesions, eosinophils have been rather neglected as possible participants to the pathogenesis of chronic urticaria because of the absence of peripheral eosinophilia in patients with this disease. However, recent data suggest a potentially relevant role played by activated eosinophils both in triggering the tissue factor pathway of coagulation cascade and as a source of vascular endothelial growth factor. Such phenomena seem more pronounced in patients showing a more severe disease. The present study will rediscuss the potential role of this cell line in chronic urticaria in the light of these recent observations.

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“…12 In rat mast cell populations, the response to thrombin is equipotent with FceRI-mediated activation. 13 Thrombin is the last enzyme of the coagulation cascade and is generated from prothrombin by activated factor X in the presence of activated factor V and calcium ions. The 2 pathways that initiate blood coagulation and lead to the activation of factor X are the contact system and the tissue factor pathway.…”

mentioning

confidence: 99%