肺線維症におけるエピモルフィンの役割(<特集>肺)

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Epimorphin was originally identified as a mesenchymal cell surface associated protein that modulates epithelial morphogenesis in embryonic organs, whereas pulmonary fibrosis is a process of wound healing, which in part mimics the process of fetal lung development. Immunohistochemical analysis showed that low levels of epimorphin were present in the bronchiolar, alveolar and vascular walls of the normal adult lungs. However, from day 7 until day 28 after bleomycin treatment, increasing levels of epimorphin immunoreactivity were detected in the mesenchymal cells and in the extracellular matrix within intra-alveolar fibrotic lesions. Moreover, Northern blots showed corresponding increases in epimorphin mRNA expression. Reepithelialization of epimorphin-rich intra-alveolar fibrosis was completed by day 28 after bleomycin, and by day 56, epimorphin immunore-activity had declined. In situ hybridization and confocal microscopic studies confirmed expression of epimorphin mRNA by mesenchymal cells situated within early fibrotic lesions, whereas immunoelectron microscopy localized the epimorphin to the endoplasmic reticulum of the mesenchymal cells and to the basement membrane and collagen fibrils in the area. In cultured mammary epithelial cells, it has been shown that epimorphin augments expression of matrix metalloproteinases (MMPs) such as gelatinase A (MMP 2) and gelatinase B (MMP 9), and both epimorphin and MMPs are required for morphogenesis. Gelatinase A and B are also known to be upregulated and activated in regenerating alveolar epithelial cells in pulmonary fibrosis. Thus, epimorphin may contribute to the remodeling of pulmonary fibrosis via epithelial-mesenchymal interactions.
日本結合組織学会の論文
2002-09-25

肺線維症におけるエピモルフィンの役割(<特集>肺)

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