| Project/Area Number |
15590802
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
CHIDA Kingo Hamamatsu University School of Medicine, Second Division Department of Internal Medicine, Associate Professor, 医学部, 助教授 (40197611)
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| Co-Investigator(Kenkyū-buntansha) |
SUDA Takafui Hamamatsu University School of Medicine, Second Division Department of Internal Medicine, Assistant Professor, 医学部, 助手 (30291397)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2004: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2003: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | idiopathic pulmonary fibrosis / control of cell cycle / fibroblast / 突発性肺線維症 / 繊維芽細胞 / 細胞周期 / RB遺伝子 / p53遺伝子 |
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| Research Abstract |
Idiopathic pulmonary fibrosis (IPF) is a progressive fibrotic disorder characterized by the proliferation of fibroblasts. Fibroblast proliferation in IPF is generally observed as a process following epithelial injury and alveolitis, but details of the mechanism remain to be clarified.
Cyclin dependent kinase (CDK) and the tumor suppressor gene, CDK inhibitor regulate cell cycle and are implicated in cell proliferation. On this basis, we hypothesized that fibroblasts in IPF have an abnormality of cell cycle regulating factors. In this report, we utilized immunohistochemistry to examine the level of expression of pRB(retinoblastoma gene product) and p27, both of which play central roles in a major tumor suppressive pathway (RB pathway), in surgically resected lung tissues of patients with IPF. The expression of pRB was reduced in fibroblastic foci compared with the adjacent tissues, while the expression of p27 did not vary. That results suggest that downregulation of pRB in fibroblastic foci contribute to the pathogenesis of IPF.
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