期刊
JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY
卷 56, 期 10, 页码 951-959出版社
SAGE PUBLICATIONS LTD
DOI: 10.1369/jhc.2008.951806
关键词
pulmonary fibrosis; lung; fibroblast foci; oxidative stress; peroxiredoxin; platelet-derived growth factor; nitrotyrosine; cell proliferation
类别
资金
- Finnish Antituberculosis Association Foundation
- Finnish Cultural Foundation
- Finnish Medical Foundation
- Pulmonary Association Heli
- Sigrid Juselius Foundation
- Yrjo Jahnsson Foundation
- health sciences research (HUCH-EVO)
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 alpha, PDGFR beta), 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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据