| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2006: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2005: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Research Abstract |
Mast cells that are differentiated in the respiratory and gut mucosa (mucosal-type mast cells : MMC) play a pivotal role in the development of allergic inflammation of the airways, nematode-induced inflammation, and worm burden clearance. We demonstrated that murine BMMC grown in the presence of IL-3 and IL-4 and the human mast cell line HMC-1 expressed E-cadherin, and BMMC cultured with a combination of four cytokines, SCF, IL-3, IL-9 and TGF-β1 expressed E-cadherin and aE67 integrin which binds to E-cadherin heterophilically. The present study aimed at elucidation of the expression and function of cell adhesion molecules included E-cadherin in mucosal type mast cells. The gene expression of BMMC cultured with a combination of SCF, IL-3, IL-9 and TGF-β1 by reserve transcription (RT)-realtime PCR showed that αEB7 integrin, Ep-CAM (Epithelial cell adhesion molecule), ZO-1 (zonula occludin) and Vinculin were upregulated. FACS analysis showed that BMMC expressed aE67 integrin and Ep-CAM at high levels. Ep-CAM is a calcium-independent homophilic cell adhesion molecule of 39-42 kDa which is expressed by the majority of epithelial tissues. ZO-1 was tight junction-associated proteins and joining to the actin cytoskeleton. Vinculin is a membrane-cytoskeletal protein in focal adhesion plaques that is involved in linkage of E-cadherin to the actin filament. These results suggest that E-cadherin, αEβ7 integrin, Ep-CAM, ZO-1 and Vinculin expressed on mucosal-type mast cells might play a critical role in cell migration, selective localization, or retention of mast cells within gut mucosa.
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