Abstract
BackgroundCatalase is preferentially expressed in bronchiolar and alveolar epithelial cells, and acts as an endogenous antioxidant enzyme in normal lungs. We thus postulated epithelial damage would be associated with a functional deficiency of catalase during the development of lung fibrosis.MethodsThe present study evaluates the expression of catalase mRNA and protein in human interstitial pneumonias and in mouse bleomycin-induced lung injury. We examined the degree of bleomycin-induced inflammation and fibrosis in the mice with lowered catalase activity.ResultsIn humans, catalase was decreased at the levels of activity, protein content and mRNA expression in fibrotic lungs (n = 12) compared to control lungs (n = 10). Immunohistochemistry revealed a decrease in catalase in bronchiolar epithelium and abnormal re-epithelialization in fibrotic areas. In C57BL/6J mice, catalase activity was suppressed along with downregulation of catalase mRNA in whole lung homogenates after bleomycin administration. In acatalasemic mice, neutrophilic inflammation was prolonged until 14 days, and there was a higher degree of lung fibrosis in association with a higher level of transforming growth factor-β expression and total collagen content following bleomycin treatment compared to wild-type mice.ConclusionsTaken together, these findings demonstrate diminished catalase expression and activity in human pulmonary fibrosis and suggest the protective role of catalase against bleomycin-induced inflammation and subsequent fibrosis.
Highlights
Catalase is preferentially expressed in bronchiolar and alveolar epithelial cells, and acts as an endogenous antioxidant enzyme in normal lungs
Arita et al recently reported that targeting of catalase directly to the mitochondria in lung epithelial cells protected the cells from hydrogen peroxide-induced apoptosis [9]
Catalase is decreased in human pulmonary fibrosis We first assessed whether the catalase activity is altered in human fibrotic lungs
Summary
Catalase is preferentially expressed in bronchiolar and alveolar epithelial cells, and acts as an endogenous antioxidant enzyme in normal lungs. Excessive hydrogen peroxide is harmful to almost all cell components, and its rapid and efficient removal is vitally important for aerobic organisms [6]. Further to this idea, in one study a transgenic mouse overexpressing catalase localized to mitochondria showed an extended life span due to enhanced protection of mitochondria from reactive oxygen species (ROS), in which catalase overexpression suppressed age-related DNA oxidation in skeletal muscle [7]. Arita et al recently reported that targeting of catalase directly to the mitochondria in lung epithelial cells protected the cells from hydrogen peroxide-induced apoptosis [9]
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