| Project/Area Number |
05454252
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
IZUMI Takateru Kyoto University Chest Disease Research Institute, Professor, 胸部疾患研究所, 教授 (80027101)
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| Co-Investigator(Kenkyū-buntansha) |
KITAICHI Masanori Chest Disease Research Institute, Associate Professor, 胸部疾患研究所, 助教授 (00161464)
MAGAI Sonoko Chest Disease Research Institute, Associate Professor, 胸部疾患研究所, 助教授 (30217955)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥6,700,000 (Direct Cost: ¥6,700,000)
Fiscal Year 1994: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1993: ¥4,700,000 (Direct Cost: ¥4,700,000)
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| Keywords | IPF / inflammation / fibrosis / fibroblast / proliferation / apoptosis / 表面抗原 / 接着因子 / 肺傷害 / 肺線維化 / 気管支肺胞洗浄液 / 肺胞上皮細胞 / 遺伝子発現 |
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| Research Abstract |
Idiopathic pulmonary fibrosis (IPF) is a chronic inflammatory interstitial lung disease with a bad prognosis. The most critical problems lie in whether the proliferative or functional characteristics of mesenchymal cells in IPF are different from those in normal lungs. In this study, we found no difference of proliferative profiles between both groups, except the discovery that the PGE2 induced suppression of proliferation of lung fibroblasts in IPF patients was lower than that of healthy controls.
In addition, we examined the life span prolongation of lung fibroblasts in IPF.we focused on whether or not lung fibroblasts from IPF patients would not undergo apoptosis which is observed in normal repair processes.
Expressions of Fas antigen and bc12 protein were examined on the tissue specimens of IPF and healthy controls by using the immunohistochemical method.The results showed no difference in expression of either protein in either of the groups. Two possibilities remain to be researched : 1.in fibroblast of IPF lungs, apoptosis occurs in the usual way, and 2.there is another putative gene which requlates apoptosis negatively.
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