title: Enhanced expression of angiotensin II type 1 receptor in usual interstitial pneumonia.
abstract: BACKGROUND
  Angiotensin II, a potent vasoconstrictor, has been considered to be involved in various fibrotic disorders including idiopathic interstitial pneumonias. To clarify whether this agent contributes to the development and progression of usual interstitial pneumonia, a major entity of idiopathic interstitial pneumonias, we immunohistochemically examined expression of its specific receptor, angiotensin II type 1 receptor, in human normal and diseased lung tissues.
  
  
  METHODS
  Video-assisted thoracoscopic lung biopsy specimens obtained from patients with usual interstitial pneumonia (n=8) were sectioned and stained using single or double immunostaining techniques with specific antibodies against angiotensin II type 1 receptor and smooth muscle actin. Lung tissues of desquamative interstitial pneumonia (n=2) and normal lung tissues (n=6) were also examined for comparative analyses.
  
  
  RESULTS
  Expression of angiotensin II type 1 receptor was limited in vascular and bronchial smooth muscle cells in normal lungs. In contrast, the receptor-positive mesenchymal cells, most of which were also positive for smooth muscle actin and arranged like a bundle, were markedly increased in association with dense collagen deposition in thickened alveolar walls of usual interstitial pneumonia. In desquamative interstitial pneumonia, the fibroproliferative change, including angiotensin II type 1 receptor-positive mesenchymal cell proliferation, was milder than that in usual interstitial pneumonia.
  
  
  CONCLUSIONS
  These findings suggest that angiotensin II and its type 1 receptor play a profibrogenic role in idiopathic interstitial pneumonias, particularly in usual interstitial pneumonia. Furthermore, angiotensin II type 1 receptor-positive smooth muscle cells increased in diseased lung tissues may be contractile and may contribute to reduction of airspaces in usual interstitial pneumonia.
authors.affiliation: Department of Pathology, Osaka City University, Graduate School of Medicine, Japan.
authors.forename: Yoshimi
authors.initials: Y
authors.lastname: Sugama
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Ikura
authors.forename: Noriko
authors.initials: N
authors.lastname: Yoshimi
authors.forename: Takehisa
authors.initials: T
authors.lastname: Suekane
authors.forename: Chizuko
authors.initials: C
authors.lastname: Kitabayashi
authors.forename: Masashi
authors.initials: M
authors.lastname: Nakagawa
authors.forename: Masahiko
authors.initials: M
authors.lastname: Ohsawa
authors.forename: Masanori
authors.initials: M
authors.lastname: Kitaichi
authors.forename: Satoru
authors.initials: S
authors.lastname: Yamamoto
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Inoue
authors.forename: Kazuto
authors.initials: K
authors.lastname: Hirata
authors.forename: Makiko
authors.initials: M
authors.lastname: Ueda
mesh_terms: D000199:Actins / Q000378:metabolism; D000328:Adult; D000368:Aged; D001706:Biopsy; D003094:Collagen / Q000378:metabolism; D005260:Female; D006801:Humans; D008168:Lung / Q000098:blood supply / Q000378:metabolism / Q000473:pathology; D017563:Lung Diseases, Interstitial / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism*
chemical_list: D000199:Actins; D044140:Receptor, Angiotensin, Type 1; D003094:Collagen