Investigation of mechanism of pulmonary fibrosis focusing on post-translational modification of osteopontin and its receptor change
Project/Area Number |
18590853
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Respiratory organ internal medicine
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Research Institution | Hiroshima University |
Principal Investigator |
YOKOSAKI Yasuyuki Hiroshima University, Health Service Center, Associate Professor (80210607)
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Co-Investigator(Kenkyū-buntansha) |
NAKATA Koh Niigata University, Medical and Dental Hospital, Professor (80207802)
MORIMOTO Yasuo Hiroshima University, University of Occupational and Environmental Health, Institute of Industrial Ecological Science, Professor (30258628)
YAMASHITA Keisuke Hiroshima University, Graduate School of Biomedical Sciences, Associate Professor (40166666)
HIGASHIKAWA Fumiko Hiroshima University, Funiko Graduate School of Biomedical Sciences, Associate Professor (70346534)
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Project Period (FY) |
2006 – 2007
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Project Status |
Completed (Fiscal Year 2007)
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Budget Amount *help |
¥4,010,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥510,000)
Fiscal Year 2007: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
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Keywords | Pulmonary Fibrosis / Osteopontin / Integrin / Neutrophil / Chemoattractant / トランスグルタミナーゼ / 重合 |
Research Abstract |
We investigated mechanism of pulmonary fibrosis focusing on post-translational modifications of osteopontin and associating receptor change. 1) Osteopontin was polymerized by transglutaminase 2. 2) Cell adhesion, spreading, and migration were enhanced when cells were plated on polymeric osteopontin than on monomeric osteopontin. 3) Focal contact formation in cells plated on polymeric osteopontin was dramatic, which suggests the cell behaviors described above were mediated by integrin receptors. 4) Polymeric osteopontin induces neutrophil migration in vitro, which was analyzed by horizontal migration analysis apparatus, Taxiscan. 5) Polymeric osteopontin recruited neutrophils into mouse peritoneal space. These results suggest that polymerization of osteopontin is involved in lung injury induced by neutrophils, the first step of pulmonary fibrosis. Although we could not describe in this report, we are on a process of generating osteopontin mutant mice to confirm the effects of polymerization of osteopontin on pulmonary fibrosis.
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Report
(3 results)
Research Products
(17 results)