title: C-Reactive Protein and Inflammatory Cytokines during Percutaneous Coronary Intervention.
abstract: BACKGROUND
  C-reactive protein (CRP) is significantly associated with cardiovascular diseases; however, whether CRP plays a causal role in coronary artery disease has yet to be determined. In addition, the relationship between CRP, atherosclerosis, and inflammation remains controversial.
  
  
  RESULTS
  Serum interleukin (IL)-6, IL-1β, and CRP levels were determined in 160 patients at time points around percutaneous coronary intervention (PCI) with drug-eluting stent implantation. The levels were found to be at peak at 24 h post-PCI and gradually declined to the level before PCI at day 30 post-PCI. These inflammation markers around PCI have no statistical difference in the different postdilation pressures (≤14, 14-18, and ≥18 atm) and stent number (1 and ≥2 stents) groups. Treatment of cultured human vascular smooth muscle cells (VSMCs) with a combination of IL-6 and IL-1β at concentrations associated with PCI did not result in any significant change in the CRP mRNA levels. The IL-6-augmented CRP expression in human internal mammary arteries (IMAs) stretched with a mechanical strength of 3 g was blocked by the nuclear factor-κB (NF-κB) peptide inhibitor SN50 and not by the inactive SN50 analog SN50M. IL-6 treatment increased NF-κB activity in human IMAs stretched with 3 g, and this effect was further blocked by stretch-activated channel (SAC) inhibitors (streptomycin or GdCl3) and SN50.
  
  
  CONCLUSIONS
  The current study provides evidence that increased serum IL-6, IL-1β, and CRP levels around PCI are not different between different postdilation pressure and stent number groups. The combination of IL-6 and IL-1β at concentrations associated with PCI cannot induce CRP expression in human VSMCs, but they can augment mechanical strain-induced CRP synthesis via the SAC-NF-κB pathway in human IMAs.
authors.affiliation: Division of Cardiology, Xiangtan Central Hospital, Xiangtan, PR China.
authors.forename: Mingxin
authors.initials: M
authors.lastname: Wu
authors.forename: Xinyuan
authors.initials: X
authors.lastname: Gu
authors.forename: Xiujuan
authors.initials: X
authors.lastname: Li
authors.forename: Yanhui
authors.initials: Y
authors.lastname: Li
authors.forename: Huaineng
authors.initials: H
authors.lastname: Zhou
authors.forename: Guihua
authors.initials: G
authors.lastname: Lu
authors.forename: ZhongKai
authors.initials: Z
authors.lastname: Wu
authors.forename: He
authors.initials: H
authors.lastname: Huang
authors.forename: Lilong
authors.initials: L
authors.lastname: Tang
authors.forename: Jianping
authors.initials: J
authors.lastname: Zeng
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000295:instrumentation; D002097:C-Reactive Protein / Q000235:genetics / Q000378:metabolism*; D002478:Cells, Cultured; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000235:genetics / Q000628:therapy*; D054855:Drug-Eluting Stents; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D053583:Interleukin-1beta / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood*; D015640:Ion Channel Gating; D007473:Ion Channels / Q000378:metabolism; D008297:Male; D008323:Mammary Arteries / Q000378:metabolism; D040542:Mechanotransduction, Cellular; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000378:metabolism; D032389:Myocytes, Smooth Muscle / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D011312:Pressure; D013314:Stress, Mechanical; D013997:Time Factors
chemical_list: C508585:IL1B protein, human; C508600:IL6 protein, human; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D015850:Interleukin-6; D007473:Ion Channels; D016328:NF-kappa B; D002097:C-Reactive Protein