| Project/Area Number |
17390242
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Teikyo University (2006-2007)
The University of Tokyo (2005) |
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Principal Investigator |
TAKIZAWA Hajime Teikyo University, The Fourth Department of Internal Medicine, Professor (80171578)
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| Co-Investigator(Kenkyū-buntansha) |
DESAKI Masashi University of Tokyo, Department of Respiratory Medicine, Research Associate (30251250)
KOHYAMA Tadashi University of Tokyo, Department of Respiratory Medicine, Lecturer (00302703)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥16,410,000 (Direct Cost: ¥15,300,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2007: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2006: ¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2005: ¥7,900,000 (Direct Cost: ¥7,900,000)
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| Keywords | smooth muscle cells / cell migration / cell signalling / myofibroblast / remodelin / epithelial mesench mal transition / cvtokine / TGFbeta / TGFβ1 / 細胞増殖 / 炎症性細胞 / 成長因子 |
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| Research Abstract |
It has been suggested that airway smooth muscle cells play important roles in the pathogenesis of asthma, but precise mechanisms remain unclear W efocused on the interactions between these structural cells and inflammatory cells such as T cells, mast cells and eosinophils Human airway smooth muscle cells express and release stem cell factor, TGF beat family molecules and and versican. These factors are believed to be chemotactic for mast cells and also be involved in airway wall remodling.IL-9, a class of Th2 type cytokine, is a potent inducer acting on airway smooth muscle cells.
Airway structural cells are once believed to be terminally differentiated cells, but recent reports strongly suggest that even these cells may change in to other type of cells. We demonstrated that human epithelial cells showed a distinct epithelial mesenchymal transition (EMT) upon stimulation of TGFbeta. These changes were induced by TNFalpha. It was suggested that dynamic interactions between airway structural cells and inflammatory cells via cytokines and growth factors play important roles in the regulation of airway remodeling in the pathogenesis of asthma. These new finding may highlight a way to develop novel type of anti-asthma drugs preventing remodeling, an irreversible airway change
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