2001 Fiscal Year Final Research Report Summary
cellular prion protein expression as a novel marker of pulmonary fibrosis and clinical significance of cellular prion proein during pulmonary fibrosis
| Project/Area Number |
12671324
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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 |
Thoracic surgery
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| Research Institution | Osaka city university |
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Principal Investigator |
INOUE Kiyotoshi Osaka city Univesity, Graduate School of Medicine, Lecturer, 大学院・医学研究科, 講師 (50193579)
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| Co-Investigator(Kenkyū-buntansha) |
KANEDA Kenji Osaka city Univesity, Graduate School of Medicine, Professor, 大学院・医学研究科, 教授 (30161186)
KINOSHITA Hiroaki Osaka city Univesity, Graduate School of Medicine, Professor, 大学院・医学研究科, 教授 (50047122)
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| Project Period (FY) |
2000 – 2001
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| Keywords | prion protein / lung / fibrosis / primary lung cancer / radiation therapy |
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| Research Abstract |
Cellular isoform of prion protein (PrPc) expression in normal and fibrotic hamster lungs. In untreated lungs, Clara cells, which were preferentially distributed in small bronchioles and characterized by globule granules, were positively stained. Reactive products were diffused in the cytoplasm outside the granules and nuclei. In bleomycin-induced pulmonary fibrosis, bronchiolar proliferation was induced in the thickened fibrous tissue around terminal bronchioles. This event was characterized by accumulation of ductular structures which were predominantly lined by PrPc positive cells representative of Clara cells. Furthermore, PrPc positive cells were occasionally populated in the epithelium of alveolar ducts and reepithelialized alveoli. These findings suggest that Clara cells might undergo proliferation and migration into acini from terminal bronchioles. The fibrous tissue contained many alpha-smooth muscle actin positive myofibroblasts. The present study indicated that PrPc is expressed in Clara cells in normal and fibrotic hamster lungs and suggests that Clara cells may proliferate as pulmonary stem cells and repair the damaged epithelium after alveolar injuries.
As clinical medical research this study aimed to evaluate the reasonable radiation area and dose for the patients who were treated with chemoradiation therapy using PrPc expression of resected specimens. But no PrPc positive cells were populated in the epithelium of alveolar ducts and reepithelialized alveoli immunohistochemically; furthermore PrPc mRNA was not detected by RT-PCR. This consequence may be caused by complete pulmonary fibrosis about 8 weeks after chemoradiation therapy. We intend to estimate the esected specimens soon after chemoradiation therapy, just before the complete pulmonary fibrosis.
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