| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Research Abstract |
ADAM10 is considered to be essential for the activation of Notch signaling. In this study, we generated mutant mice in which Adam10 is disrupted under the control of an inducible Mx1-Cre transgene (A10/Mx1 mice) and aimed to elucidate the potential functions of ADAM10-Notch signaling in bone metabolism. A10/Mx1 mice exhibited the increase in population of Gr-1+CD11b+ cells and hematopoietic stem cells. Furthermore, lack of ADAM10 in the non-hematopoietic cells lead to aberrant production of G-CSF. These results revealed that ADAM10-Notch signaling negatively regulates the production of G-CSF in non-hematopoietic cells and indirectly suppresses myelopoiesis in a non-cell-autonomous manner. On the other hand, A10/Mx1 mice exhibited an increase of osteoclast progenitor cells in the bone marrow, and many osteocalcin+ cells, a marker for mature osteoblast, existed on the trabecular bone. This result suggests A10/Mx1 mice accelerated not only bone resorption but also bone formation.
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