Loss of Caveolin-1 in Bronchiolization in Lung Fibrosis
Nao Odajima 1, Tomoko Betsuyaku 1*, Yasuyuki Nasuhara 1 and Masaharu Nishimura 1
1 First Department of Medicine, Hokkaido University School of Medicine, Sapporo, Japan
* To whom correspondence should be addressed. E-mail: bytomoko{at}med.hokudai.ac.jp.
Submitted on February 1, 2007
Accepted on 9 April 2007
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Abstract |
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Bronchiolization is a key process in fibrosing lung in which the proliferative status of bronchiolar epithelium changes, leading to abnormal epithelial morphology. Within the context that caveolin-1 acts to suppress epithelial proliferation, we postulated that stimulating epithelial injury would lead to caveolin-1 downregulation and encourage proliferation. The present study evaluates the expression of caveolin-1, especially in bronchiolization, in C57BL/6J mice with bleomycin-induced lung fibrosis and in various types of re-epithelialization in human interstitial pneumonias (IPs). Immunohistochemically the levels of caveolin-1 decreased in the bronchiolar epithelium of mice treated with bleomycin. Levels of caveolin-1 mRNA in the whole lung were decreased at 7 and 14 days. Caveolin-1 mRNA was also decreased in laser capture microdissection- retrieved bronchiolar epithelial cells at 7 days. Among patients with 12 IPs including 4 usual IP (UIP) and 8 nonspecific IP (NSIP), whole lung caveolin-1 was significantly decreased compared with 12 controls at both mRNA and protein levels. By scoring immunointensity, caveolin-1 was significantly reduced in bronchiolization and squamous metaplasia as well as in bronchiolar epithelium in 23 IPs (12 UIP and 11 NSIP) compared with bronchiolar epithelium from 7 controls. These data suggested the loss of caveolin-1 is associated with abnormal re-epithelialization in lung fibrosis.
Key Words:
caveolin-1, bleomycin, lung fibrosis, bronchiolization, laser capture microdissection
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