title: [Contribution of monocyte chemoattractant protein-1 and c-fms/macrophage colony-stimulating factor receptor to coronary artery disease: analysis of human coronary atherectomy specimens].
abstract: OBJECTIVE
  Primary coronary atherosclerotic lesions(de novo lesions) are a type of inflammatory vascular disease. Restenotic lesions after percutaneous coronary intervention mainly consist of proliferative vascular smooth muscle cells. Recent studies have demonstrated that locally synthesized cytokines, including chemokines, are important in both these coronary lesions. Monocyte chemoattractant protein(MCP)-1 and macrophage colony-stimulating factor(M-CSF) are two of the associated chemokines, but their role in coronary artery disease has not been sufficiently clarified. This study investigated the expression of MCP-1 and c-fms/M-CSF receptor in human coronary tissues.
  
  
  METHODS
  Histological and immunohistochemical studies used samples obtained from patients who underwent directional coronary atherectomy(28 de novo lesions and 16 restenotic lesions). The following primary antibodies were used: anti-MCP-1, anti-c-fms, anti-macrophages and anti-alpha-smooth muscle actin.
  
  
  RESULTS
  Focal accumulation of macrophage-derived foam cells, thrombus, cholesterol clefts and calcification tended to be more frequent in de novo lesions than in restenotic lesions. On the other hand, restenotic lesions mainly consisted of stellate vascular smooth muscle cells and extracellular matrix. The expression of MCP-1-positive cells almost coincided with the macrophages. In contrast, staining for MCP-1 was little seen in the stellate vascular smooth muscle cells. Expression of c-fms was found in both macrophages and stellate vascular smooth muscle cells. Expression patterns of MCP-1 and c-fms exhibited no difference between the two lesion types.
  
  
  CONCLUSIONS
  Both MCP-1 and the M-CSF/c-fms system are involved in the atherogenesis of de novo lesions. However, the M-CSF/c-fms system, rather than MCP-1, is more important in the late stage of restenosis.
authors.affiliation: Third Department of Internal Medicine, Showa University School of Medicine, Hatanodai 1-5-8, Shinagawa-ku, Tokyo 142-8666.
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Iso
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Suzuki
authors.forename: Takatoshi
authors.initials: T
authors.lastname: Sato
authors.forename: Makoto
authors.initials: M
authors.lastname: Shoji
authors.forename: Masayuki
authors.initials: M
authors.lastname: Shibata
authors.forename: Yuji
authors.initials: Y
authors.lastname: Hamazaki
authors.forename: Shinji
authors.initials: S
authors.lastname: Koba
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Sakai
authors.forename: Mikitaka
authors.initials: M
authors.lastname: Murakami
authors.forename: Eiichi
authors.initials: E
authors.lastname: Geshi
authors.forename: Takashi
authors.initials: T
authors.lastname: Katagiri
mesh_terms: D000368:Aged; D017225:Atherectomy, Coronary; D018932:Chemokine CCL2 / Q000096:biosynthesis / Q000502:physiology*; D003324:Coronary Artery Disease / Q000378:metabolism / Q000473:pathology* / Q000601:surgery; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D016186:Receptor, Macrophage Colony-Stimulating Factor / Q000096:biosynthesis / Q000502:physiology*
chemical_list: D018932:Chemokine CCL2; D016186:Receptor, Macrophage Colony-Stimulating Factor