title: C-reactive protein promotes vascular endothelial dysfunction partly via activating adipose tissue inflammation in hyperlipidemic rabbits.
abstract: BACKGROUND
  Endothelial dysfunction is the basic and original sign of atherogenesis. Some evidences show that C-reactive protein (CRP) and perivascular adipose tissue (PVAT) play a pivotal role in atherosclerosis. However, the effects of CRP on atherosclerosis and the related mechanisms require elucidation.
  
  
  METHODS
  The levels of basic total cholesterol, low-density lipoprotein cholesterol, triglyceride, CRP, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), nitric oxide (NO) and endothelin-1 (ET-1) were respectively measured in rabbits, endothelium-dependent vasorelaxation function was also evaluated. Animals were randomly divided into two groups: PVAT(-) and PVAT(+) group (removing or keeping pericarotid adipose tissue (PCAT)). Both of the two groups were exposed to a high-fat diet for six-week, and then sustained CRP treatment was performed for a week, at this time point all the above parameters were remeasured. In addition, mRNA and protein expression of TNF-α, IL-6, and macrophage chemoattractant protein-1 (MCP-1) were respectively evaluated by Polymerase Chain Reaction and immunoblotting in PCAT and cultured adipocytes treated by CRP.
  
  
  RESULTS
  High-fat diet greatly increased the serum lipids and inflammatory markers, induced endothelial dysfunction and imbalance between NO and ET-1, increased mRNA and protein expression of TNF-α, IL-6, MCP-1 and enhanced macrophage infiltration of PCAT. CRP treatment could further promote macrophage infiltration of PVAT, induce the imbalance between NO and ET-1, aggravate endothelial dysfunction especially in PVAT(+) arteries, and could also enhance the above-mentioned mRNA and protein expression in PCAT and cultured adipocytes.
  
  
  CONCLUSIONS
  CRP could significantly promote endothelial dysfunction in high-fat diet rabbits especially in PVAT(+) groups, which may be partly mediated by activating inflammatory reaction of adipose tissue.
authors: Department of Cardiology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, 510120, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Guangzhou, 510120, China.
authors: YangXin
authors: Y
authors: Chen
authors: XiaoQiao
authors: X
authors: Wang
authors: JingTing
authors: J
authors: Mai
authors: XiaoMiao
authors: X
authors: Zhao
authors: YongHong
authors: Y
authors: Liang
authors: MiaoNing
authors: M
authors: Gu
authors: ZhongQing
authors: Z
authors: Chen
authors: RuQiong
authors: R
authors: Nie
authors: JingFeng
authors: J
authors: Wang
mesh_terms: D000273:Adipose Tissue; D000818:Animals; D001808:Blood Vessels; D002097:C-Reactive Protein / Q000502:physiology*; D059305:Diet, High-Fat; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006949:Hyperlipidemias / Q000150:complications*; D007249:Inflammation / Q000209:etiology*; D008297:Male; D011817:Rabbits
chemical_list: D002097:C-Reactive Protein
keywords: Adipose tissue; C-reactive protein; Endothelial dysfunction; Inflammation