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Citations to this article

Increased vascular permeability in C1 inhibitor–deficient mice mediated by the bradykinin type 2 receptor
Eun D. Han, … , Jennifer Scafidi, Alvin E. Davis III
Eun D. Han, … , Jennifer Scafidi, Alvin E. Davis III
Published April 15, 2002
Citation Information: J Clin Invest. 2002;109(8):1057-1063. https://doi.org/10.1172/JCI14211.
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Article Immunology

Increased vascular permeability in C1 inhibitor–deficient mice mediated by the bradykinin type 2 receptor

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Abstract

Heterozygosity for C1 inhibitor (C1INH) deficiency results in hereditary angioedema. Disruption of the C1INH gene by gene trapping enabled the generation of homozygous- and heterozygous-deficient mice. Mating of heterozygous-deficient mice resulted in the expected 1:2:1 ratio of wild-type, heterozygous, and homozygous-deficient offspring. C1INH-deficient mice showed no obvious phenotypic abnormality. However, following injection with Evans blue dye, both homozygous and heterozygous C1INH-deficient mice revealed increased vascular permeability in comparison with wild-type littermates. This increased vascular permeability was reversed by treatment with intravenous human C1INH, with a Kunitz domain plasma kallikrein inhibitor (DX88), and with a bradykinin type 2 receptor (Bk2R) antagonist (Hoe140). In addition, treatment of the C1INH-deficient mice with an angiotensin-converting enzyme inhibitor (captopril) increased the vascular permeability. Mice with deficiency of both C1INH and Bk2R demonstrated diminished vascular permeability in comparison with C1INH-deficient, Bk2R-sufficient mice. These data support the hypothesis that angioedema is mediated by bradykinin via Bk2R.

Authors

Eun D. Han, Ryan C. MacFarlane, Aideen N. Mulligan, Jennifer Scafidi, Alvin E. Davis III

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Year: 2025 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 2008 2007 2006 2005 2004 2002 Total
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