Enhanced expression of angiotensin II type 1 receptor in usual interstitial pneumonia.
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.
Sugama
Yoshimi
Y
Department of Pathology, Osaka City University, Graduate School of Medicine, Japan.
Ikura
Yoshihiro
Y
Yoshimi
Noriko
N
Suekane
Takehisa
T
Kitabayashi
Chizuko
C
Nakagawa
Masashi
M
Ohsawa
Masahiko
M
Kitaichi
Masanori
M
Yamamoto
Satoru
S
Inoue
Yoshikazu
Y
Hirata
Kazuto
K
Ueda
Makiko
M
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*
D000199:Actins; D044140:Receptor, Angiotensin, Type 1; D003094:Collagen