title: Immunohistochemical properties in the patients with Buerger's disease--possible role of plasminogen activator inhibitor-1 for preservation of vessel wall architecture.
abstract: BACKGROUND
  The architecture of the arterial wall affected with Buerger's disease has been known to be preserved in all three layers, while the one affected by arteriosclerosis obliterans (ASO) is degenerated and destroyed. We analyzed affected arteries with immunohistochemical methods to clarify the differences between Buerger's disease and ASO.
  
  
  METHODS
  Crural arteries obtained from 13 patients with Buerger's disease and 6 patients with ASO at our institute were studied. In addition, we examined seven specimens from six patients who were thought to be normal (without Buerger's disease or ASO) as negative control. Immunohistochemical studies were performed on paraffin-embedded tissues. The primary antibodies were urokinase-type plasminogen activator (uPA) and matrix metalloproteinase-3 (MMP-3). Both are known to play an important role of extracellular proteolysis and to activate each other. Additionally, plasminogen activator inhibitor-1(PAI-1) was also examined.
  
  
  RESULTS
  In Buerger's disease, PAI-1 was well expressed along the internal elastic lamina. Urokinase-type plasminogen activator and MMP-3 were slightly positive in intima and media. In ASO, a slight amount of PAI-1 was recognized on vessel walls, and both uPA and MMP-3 were strongly positive in media. In addition, in the control group, PAI-1, uPA, and MMP-3 were well expressed in media.
  
  
  CONCLUSIONS
  In Buerger's disease, PAI-1 was strongly expressed around the internal elastic lamina, while both uPA and MMP-3 were slightly recognized on vessel walls. These findings could be one of the reasons the general architecture of vessel walls in Buerger's disease is preserved.
authors: Division of Vascular Surgery, Department of Surgery, Nagoya University Graduate School of Medicine, Japan. sato-toshimitsu@pref.gifu.lg.jp
authors: Toshimitsu
authors: T
authors: Sato
authors: Hiroaki
authors: H
authors: Tamai
authors: Masayoshi
authors: M
authors: Kobayashi
authors: Kiyohito
authors: K
authors: Yamamoto
authors: Kimihiro
authors: K
authors: Komori
mesh_terms: D000328:Adult; D001158:Arteries / Q000378:metabolism / Q000473:pathology*; D001162:Arteriosclerosis Obliterans / Q000378:metabolism / Q000473:pathology; D015415:Biomarkers / Q000378:metabolism; D002114:Calcinosis / Q000378:metabolism / Q000473:pathology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D019278:Matrix Metalloproteinase 3 / Q000378:metabolism; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism*; D013919:Thromboangiitis Obliterans / Q000378:metabolism / Q000473:pathology*; D014568:Urokinase-Type Plasminogen Activator / Q000378:metabolism
chemical_list: D015415:Biomarkers; D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human; D014568:Urokinase-Type Plasminogen Activator; D019278:Matrix Metalloproteinase 3