Role of the B1 bradykinin receptor and gC1qR/p33 in angioedema.

Abstract

Patients affected by angioedema (AE) are subject to asymmetric, nonerythematous, nonpruritic, localized, transient, episodic swelling of deeper layers or submucosal tissues of the skin, oropharyngolaryngeal tissue, and/or gastrointestinal wall. The nonapeptide bradykinin (BK) may be largely responsible for the vascular permeability seen in most AE. During AE attacks, activation of the serine proteases leads to the release of BK. Enzymes expressed on the endothelial cell membrane can metabolize BK, producing the agonist of the B1R, which can then be upregulated by proinflammatory stimuli, suggesting that the blockade of B1R and B2R, or gC1q/p33, may provide novel therapeutic targets.

• Authors: Fleur Bossi, Francesco Tedesco
• Journal: Immunology and allergy clinics of North America (Immunol Allergy Clin North Am) Vol. 33 Issue 4 Pg. 535-44 (Nov 2013) ISSN: 1557-8607 [Electronic] United States
• PMID: 24176217 (Publication Type: Journal Article, Review)
• Copyright: Copyright © 2013 Elsevier Inc. All rights reserved.

Chemical References

• C1QBP protein, human
• Carrier Proteins
• Mitochondrial Proteins
• Receptor, Bradykinin B1
• Bradykinin

Topics

• Angioedema (diagnosis, metabolism)
• Bradykinin (metabolism)
• Carrier Proteins (metabolism)
• Endothelial Cells (metabolism)
• Humans
• Mitochondrial Proteins (metabolism)
• Receptor, Bradykinin B1 (metabolism)