title: C-reactive protein reduces protein S-nitrosylation in endothelial cells.
abstract: C-reactive protein (CRP) emerges as an important mediator of cardiovascular lesions. In this study, we aimed to assess the role of CRP in the S-nitrosylation of proteins in endothelial cells and elucidate the potential mechanisms. Our results showed that CRP reduced protein S-nitrosylation in human umbilical vein endothelial cells (HUVECs). NO donor S-nitrosoglutathione antagonized CRP-mediated reduction of protein S-nitrosylation. Neutralizing antibody to Fcγ receptor II remarkably attenuated these changes. In addition, CRP increased NF-κB activation via the reduction of S-nitrosylation of p65, but not p50 in HUVECs, and induced the upregulation of NF-kB target gene vascular cell adhesion molecule-1. Furthermore, we confirmed that CRP reduced S-nitrosylated proteins in the rat aorta. Taken together, these data suggest that CRP-induced decline of protein S-nitrosylation by activating NF-κB via reduction of S-nitrosylation of p65, which may contribute to the endothelial dysfunction.
authors.affiliation: Department of Cardiovascular Medicine, First Affiliated Hospital of Medical College, Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, 710061 Shaanxi, China.
authors.forename: Xinhong
authors.initials: X
authors.lastname: Wang
authors.forename: Weimin
authors.initials: W
authors.lastname: Liu
authors.forename: Yue
authors.initials: Y
authors.lastname: Wu
authors.forename: Xiaojun
authors.initials: X
authors.lastname: Liu
authors.forename: Xiao
authors.initials: X
authors.lastname: Liang
authors.forename: Zhaofei
authors.initials: Z
authors.lastname: Wan
authors.forename: Nanping
authors.initials: N
authors.lastname: Wang
authors.forename: Zuyi
authors.initials: Z
authors.lastname: Yuan
mesh_terms: D000818:Animals; D001011:Aorta / Q000378:metabolism; D002097:C-Reactive Protein / Q000502:physiology*; D002478:Cells, Cultured; D003545:Cysteine / Q000031:analogs & derivatives* / Q000378:metabolism; D061307:Human Umbilical Vein Endothelial Cells / Q000378:metabolism*; D006801:Humans; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D020030:Nitric Oxide Donors / Q000494:pharmacology; D011499:Protein Processing, Post-Translational; D051381:Rats; D017207:Rats, Sprague-Dawley; D017452:Receptors, IgG / Q000378:metabolism; D026422:S-Nitrosoglutathione / Q000494:pharmacology; D026403:S-Nitrosothiols / Q000378:metabolism*; D051996:Transcription Factor RelA / Q000378:metabolism
chemical_list: C445323:FCGR2A protein, human; C499173:FCGR2B protein, human; D020030:Nitric Oxide Donors; C498143:RELA protein, human; D017452:Receptors, IgG; D026403:S-Nitrosothiols; D051996:Transcription Factor RelA; D009569:Nitric Oxide; D026422:S-Nitrosoglutathione; D002097:C-Reactive Protein; C021315:S-nitrosocysteine; D003545:Cysteine