title: Potential involvement of CCL23 in atherosclerotic lesion formation/progression by the enhancement of chemotaxis, adhesion molecule expression, and MMP-2 release from monocytes.
abstract: OBJECTIVE
  CCL23 [Ckβ8-1/myeloid progenitor inhibitory factor 1 (MPIF1)/macrophage inflammatory protein-3 (MIP3)], a member of the CC chemokine family, is involved in leukocyte trafficking, and implicated in inflammatory diseases. In the present study, we investigated the role of CCL23 in the development of human atherosclerosis, which is characterized by an inflammatory disease.
  
  
  METHODS
  CCL23 transcripts were measured by reverse transcriptase-polymerase chain reaction (RT-PCR) and CCL23 protein by immunohistochemistry and enzyme-linked immunosorbent assay (ELISA). Expression of adhesion molecules was determined by flow cytometry, and matrix metalloproteinase-2 (MMP-2) levels by zymography.
  
  
  RESULTS
  Proatherogenic factors such as oxidized low-density lipoprotein (oxLDL) and oxidative stress markedly enhanced CCL23 release from human THP-1 macrophages. CCL23 stimulated chemotaxis of human THP-1 monocytes in a dose-dependent manner and enhanced the expression of adhesion molecule CD11c, as well as release of MMP-2 from the THP-1 monocytes. Moreover, CCL23 expression at the mRNA level was significantly higher in human atherosclerotic lesions than in normal arteries, and CCL23 protein was co-expressed with CD68, a specific marker for macrophages. Circulating levels of plasma CCL23 were higher in atherosclerotic patients than in normal subjects.
  
  
  CONCLUSIONS
  These findings suggest that CCL23 plays a role in the development of human atherosclerosis. CCL23 may be a useful target for the development of antiatherogenic agents.
authors.affiliation: Department of Food Science and Nutrition, University of Ulsan, Ulsan, 680-749, South Korea.
authors.forename: Chu-Sook
authors.initials: CS
authors.lastname: Kim
authors.forename: Ji-Hye
authors.initials: JH
authors.lastname: Kang
authors.forename: Hong-Rae
authors.initials: HR
authors.lastname: Cho
authors.forename: Thomas N
authors.initials: TN
authors.lastname: Blankenship
authors.forename: Kent L
authors.initials: KL
authors.lastname: Erickson
authors.forename: Teruo
authors.initials: T
authors.lastname: Kawada
authors.forename: Rina
authors.initials: R
authors.lastname: Yu
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000097:blood / Q000276:immunology* / Q000473:pathology*; D039521:CD11c Antigen / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000378:metabolism; D019742:Chemokines, CC / Q000097:blood / Q000235:genetics / Q000276:immunology*; D002633:Chemotaxis / Q000502:physiology*; D005260:Female; D006801:Humans; D008077:Lipoproteins, LDL / Q000378:metabolism; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism*; D009000:Monocytes / Q000166:cytology / Q000378:metabolism*; D018384:Oxidative Stress
chemical_list: C111835:CCL2 protein, human; C105504:CCL23 protein, human; D039521:CD11c Antigen; D015815:Cell Adhesion Molecules; D018932:Chemokine CCL2; D019742:Chemokines, CC; D008077:Lipoproteins, LDL; C099252:oxidized low density lipoprotein; D020778:Matrix Metalloproteinase 2