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Peroxiredoxin II Expression and Its Association With Oxidative Stress and Cell Proliferation in Human Idiopathic Pulmonary Fibrosis

Kirsi Vuorinen, Steffen Ohlmeier, Outi Leppäranta, Kaisa Salmenkivi, Marjukka Myllärniemi and Vuokko L. Kinnula

Pulmonary Division, Department of Medicine (KV,OL,MM,VLK) and Department of Pathology (KS), University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland, and Department of Biochemistry, Proteomics Core Facility, Biocenter Oulu, University of Oulu, Oulu, Finland (SO)

Correspondence to: Vuokko L. Kinnula, University of Helsinki, Department of Medicine, PO Box 22, FI-00014 Helsinki, Finland. E-mail: vuokko.kinnula{at}helsinki.fi

Oxidant burden has been suggested to be a contributor to the pathogenesis of idiopathic pulmonary fibrosis (IPF). The study focused on peroxiredoxin (Prx) II, an antioxidant that has been associated with platelet-derived growth factor (PDGF) signaling and consequent cell proliferation. Localization and expression of Prx II, PDGF receptors (PDGFR, PDGFRβ), Ki67, and nitrotyrosine were assessed in control (n=10) and IPF/usual interstitial pneumonia (UIP) (n=10) lung biopsies by immunohistochemistry and morphometry. Prx II oxidation was determined by standard and non-reducing Western blots, two-dimensional gel electrophoresis, and mass spectrometry. Prx II localized in the IPF/UIP epithelium and alveolar macrophages. Prx II–positive area in the fibroblastic foci (FF) was smaller than in other parenchymal areas (p=0.03) or in the hyperplastic epithelium (p=0.01). There was no major Prx II oxidation in IPF/UIP compared with the normal lung. The FF showed only minor immunoreactivity to the PDGFRs; Ki67, a marker of cell proliferation; and nitrotyrosine, a marker of oxidative/nitrosative stress. The results suggest that Prx II oxidation does not relate to the pathogenesis of IPF/UIP and that Prx II, PDGFRs, and proliferating cells colocalize in the IPF/UIP lung. Unexpectedly, FF represented areas of low cell proliferation. (J Histochem Cytochem 56:951–959, 2008)

Key Words: pulmonary fibrosis • lung • fibroblast foci • oxidative stress • peroxiredoxin • platelet-derived growth factor • nitrotyrosine • cell proliferation

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