The Hyaluronan-Binding Serine Protease from Human Plasma Cleaves HMW and LMW Kininogen and Releases Bradykinin

Etscheid, Michael; Beer, Nicole; Fink, Edwin; Seitz, Rainer; Dodt, Johannes

doi:10.1515/bc.2002.184

Cited by 37 publications

(29 citation statements)

References 43 publications

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“…Other substrates for FSAP include; pro-uPA 51,52 , fibrinogen and fibronectin 52 , TFPI 53 , PDGF-BB 54 , bFGF/EGF 55 and kininogen 49,56 . In addition FSAP degrades histones from necrotic In patients with carotid stenosis, the presence of the MI-SNP was associated with a worse outcome 68 .…”

Section: Functions Of Fsapmentioning

confidence: 99%

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Factor VII activating protease (FSAP) regulates the expression of inflammatory genes in vascular smooth muscle and endothelial cells

et al. 2017

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Section: Functions Of Fsapmentioning

confidence: 99%

“…Additional FSAP was also shown to cleave kininogen and thereby release bradykinin, suggesting yet another cellular activation mechanism 56 .…”

Section: Cellular Effects Of Fsapmentioning

confidence: 99%

Factor VII activating protease (FSAP) regulates the expression of inflammatory genes in vascular smooth muscle and endothelial cells

et al. 2017

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“…Plasmin at high concentration in turn has been shown to activate FXII and hence may therefore theoretically contribute to CP mediated BK generation (12,29). Factor VII-activating protease (FSAP), which is activated upon contact with dead cells, has been demonstrated induce BK generation from HK; however the contribution to BK formation in vivo is not established yet (30,31). Tissue kallikrein 1 (KLK1) has been shown to induce LK cleavage resulting in the liberation of Lys-BK, which may subsequently processed to BK by aminopeptidases (32,33).…”

Section: Clinical Picturementioning

confidence: 99%

Hereditary and acquired C1-inhibitor-dependent angioedema: from pathophysiology to treatment

Zeerleder

Levi

2016

Annals of Medicine

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Uncontrolled generation of bradykinin (BK) due to insufficient levels of protease inhibitors controlling contact phase (CP) activation, increased activity of CP proteins, and/or inadequate degradation of BK into inactive peptides increases vascular permeability via BK-receptor 2 (BKR2) and results in subcutaneous and submucosal edema formation. Hereditary and acquired angioedema due to C1-inhibitor deficiency (C1-INH-HAE and -AAE) are diseases characterized by serious and potentially fatal attacks of subcutaneous and submucosal edemas of upper airways, facial structures, abdomen, and extremities, due to inadequate control of BK generation. A decreased activity of C1-inhibitor is the hallmark of C1-INH-HAE (types 1 and 2) due to a mutation in the C1-inhibitor gene, whereas the deficiency in C1-inhibitor in C1-INH-AAE is the result of autoimmune phenomena. In HAE with normal C1-inhibitor, a significant percentage of patients have an increased activity of factor XIIa due to a FXII mutation (FXII-HAE). Treatment of C1-inhibitordependent angioedema focuses on restoring control of BK generation by inhibition of CP proteases by correcting the balance between CP inhibitors and BK breakdown or by inhibition of BK-mediated effects at the BKR2 on endothelial cells. This review will address the pathophysiology, clinical picture, diagnosis and available treatment in C1-inhibitor-dependent angioedema focusing on BK-release and its regulation. ä KEY MESSAGESInadequate control of bradykinin formation results in the formation of characteristic subcutaneous and submucosal edemas of the skin, upper airways, facial structures, abdomen and extremities as seen in hereditary and acquired C1-inhibitor-dependent angioedema. Diagnosis of hereditary and acquired C1-inhibitor-dependent angioedema may be troublesome as illustrated by the fact that there is a significant delay in diagnosis; a certain grade of suspicion is therefore crucial for quick diagnosis. Submucosal edema formation in hereditary and acquired C1-inhibitor-dependent angioedema is potentially life threatening and can occur at any age. To date effective therapies for acute and prophylactic treatment are available. ARTICLE HISTORY

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“…In addition, PHBP is active in releasing the vasoactive peptide bradykinin, through a cleavage of kininogen [8]. The PHBP mutant with Gly 511 substituted by Glu (Marburg I polymorphism) has a weaker activity in single-chain u-PA activation, but the same activity in FVII activation compared with the wild-type enzyme [9].…”

Section: Introductionmentioning

confidence: 99%

Polyamine‐promoted autoactivation of plasma hyaluronan‐binding protein

Yamamichi¹,

Nishitani²,

Nishimura³

et al. 2010

Journal of Thrombosis and Haemostasis

115

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The Hyaluronan-Binding Serine Protease from Human Plasma Cleaves HMW and LMW Kininogen and Releases Bradykinin

Cited by 37 publications

References 43 publications

Factor VII activating protease (FSAP) regulates the expression of inflammatory genes in vascular smooth muscle and endothelial cells

Factor VII activating protease (FSAP) regulates the expression of inflammatory genes in vascular smooth muscle and endothelial cells

Hereditary and acquired C1-inhibitor-dependent angioedema: from pathophysiology to treatment

Polyamine‐promoted autoactivation of plasma hyaluronan‐binding protein

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