| Project/Area Number |
08670676
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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 | Dokkyo Univ.Sch.of Med. |
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Principal Investigator |
MOTOJIMA Shinji Dokkyo Univ Sch Med Intern Med, Ass.Prof., 医学部, 助教授 (90157842)
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| Co-Investigator(Kenkyū-buntansha) |
HIRATA Akira Dokkyo Univ Sch Med Intern Med, Instructor, 医学部, 助手 (00218778)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1997: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1996: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | airway epithelium / eosinophil / GM-CSF / eosinphil peroxidase / major basic protein / tyrosine phosphorylation / Eosinophil Perondase / Granulocyte-macrophage colony-stimulatir,factor / 気道上皮細胞 / 顆粒蛋白 |
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| Research Abstract |
In the study of the previous year, we have found that eosinophil-derived basic proteins, namely eosinophil peroxidase (EPO) and major basic protein (MBP), stimulate the release of granulocyte-macrophage colony-stimulating factor (GM-CSF) from bronchial epithelial cells. This year we studied whether tyrosine phosphorylation is involved in the release of GM-CSF.The bronchial epithelial cells were stimulated with EPO (5.9x 10^<-7>M) in the presence or absence of tyrosine phosphorylation inhibitor, herbimycin A (0.2-2.0mug/ml) or genistein (10-100mug/ml), and the release of GM-CSF was evaluated. Both of the tyrosine phosphorylation inhibitors inhibited the release of GM-CSF from the epithelial cells in a concentration-dependent manner. Moreover, the GM-CSF release with IL-1beta and TNF-alpha, very potent stimuli for GM-CSF release, was also completely inhibited with these inhibitors. The proteins which are tyrosine-phosphorylated in terms of molecular weight revealed the same in the stimulation of IL-1beta and EPO by the use of Western blot. Although the GM-CSF release by EPO or MBP does not seem to involve specific receptors, the same signal transduction pathway seems to be utilized as in the case of IL-1beta which has a specific receptor. Further studies are needed to specify the proteins which are tyrosine-phosphorylated and to clarify the signal transduction of EPO and MBP in bronchial epithelial cells in the absence of a specific receptor.
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