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Expression of Osteopontin in a Macrophage Cell Line and in Transgenic Mice with Pulmonary Fibrosis Resulting from the Lung Expression of a Tumor Necrosis Factor‐α Transgene
Author(s) -
MIYAZAKI YOSHITAKA,
TASHIRO TAKAYOSHI,
HIGUCHI YASUNORI,
SETOGUCHI MIHOKO,
YAMAMOTO SHUNSUKE,
NAGAI HIROYUKI,
NASU MASARU,
VASSALLI PIERRE
Publication year - 1995
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1995.tb44651.x
Subject(s) - osteopontin , transgene , pulmonary fibrosis , tumor necrosis factor alpha , cancer research , macrophage , genetically modified mouse , lung , fibrosis , cell culture , biology , medicine , pathology , immunology , gene , genetics , in vitro
The expression level of osteopontin (OPN) mRNA was found to be increased in a macrophage cell line in the presence of recombinant tumor necrosis factor-alpha (TNF-alpha). OPN mRNA level was also explored in the lungs of transgenic mice which were expressing TNF-alpha in type II pneumocytes, a condition leading to pulmonary alveolitis and progressive fibrosis. OPN mRNA was significantly increased in the lungs of these transgenic mice. In situ hybridization showed that it was localized mostly in alveolar macrophages. Since OPN can be induced in macrophages by TNF-alpha stimulation and since on the other hand osteopontin appears to decrease the level of nitric oxide synthase, and thus the production of nitric oxide, osteopontin might also indirectly have an antifibrotic effect. The role played by osteopontin in fibrotic lesions resulting from the release of TNF-alpha deserves further study, since it may be involved in the balance of opposite effects eventually leading to local tissue damage ending in fibrosis.