Open AccessCoupling of Fcγ Receptor I to Fcγ Receptor IIB by Src Kinase Mediates C-Reactive Protein Impairment of Endothelial Function
Author(s) -
Nathan C. Sundgren,
Weifei Zhu,
Ivan S. Yuhanna,
Ken L. Chambliss,
Mohamed Ahmed,
Keiji Tanigaki,
Michihisa Umetani,
Chieko Mineo,
Philip W. Shaul
Publication year - 2011
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/circresaha.111.254573
Subject(s) - enos , receptor , medicine , endocrinology , tyrosine phosphorylation , proto oncogene tyrosine protein kinase src , endothelium , chemistry , fc receptor , biology , nitric oxide , nitric oxide synthase
Elevations in C-reactive protein (CRP) are associated with increased cardiovascular disease risk and endothelial dysfunction. CRP antagonizes endothelial nitric oxide synthase (eNOS) through processes mediated by the IgG receptor Fcγ receptor IIB (FcγRIIB), its immunoreceptor tyrosine-based inhibitory motif, and SH2 domain-containing inositol 5'-phosphatase 1. In mice, CRP actions on eNOS blunt carotid artery re-endothelialization.
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