| Project/Area Number |
16300200
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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 |
Sports science
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| Research Institution | Akita University |
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Principal Investigator |
NANJO Hiroshi Akita University, School of Medicine, lecturer, 医学部, 講師 (70250892)
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| Co-Investigator(Kenkyū-buntansha) |
MASUDA Hirotake Akita University, School of Medicine, professor, 医学部, 教授 (60103462)
KAWAMURA Koichi Akita University, School of Medicine, associated professor, 医学部, 助教授 (00091801)
TAKAHASHI Masato Akita University, School of Medicine, assistant, 医学部, 助手 (10315806)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥7,100,000 (Direct Cost: ¥7,100,000)
Fiscal Year 2005: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 2004: ¥5,200,000 (Direct Cost: ¥5,200,000)
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| Keywords | bone marrow-derived cell / endothelial cell / vascular remodeling / Intimal thickening / CD34-positive cells / wall shear stress / aortic aneurysm / training / 毛細血管 / 心筋 / 骨格筋 / 骨髄キメラ / 脳 / リモデリング / 心臓 / 血管 / 血流 |
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| Research Abstract |
1)Hemodynamic conditions influenced CD34-positive cell localization and differentiation inexperimental abdominal aortic aneurysm. Adventitial capillary angiogenesis may augment inflammation and disease progression. Modulating cell lineage differentiation of mature progenitor cells may represent a novel therapeutic atrategy to maintain medial cellularity and extracellular matrix integrity in abdominal aortic aneurysm disease.
2)Endothelial cells, which had once been stimulated by high flow, transiently proliferated even after normalization of high-flow or removal of flow. Proliferation of endothelial cells may be promised when they start to proliferate after high-flow loading.
3)Flow differentially regulates cell-specific abdominal aortic aneurysm gene expression. Cell-type specific expression and functional analyses may substantially clarify the pathophysiology of abdominal aortic aneurysm disease.
4)Repeated, intermittent short-duration exposure to low shear stress in the setting of high
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flow and high shear stress can induce arterial intimal thickening. Short-duration alterations in hemodynamic forces induce rapid vascular cell message expression, which may effect arterial remodeling. A threshold value of 5 dyn/cm^2 may be needed in order to initiate and sustain the iintimal thickening response.
5)Bone marrow-derived endothelial cells were present mainly in the capillaries of all organs. Bone marrow-derived endothelial cells in the heart were approximate 50-100 times as many as them in the skeletal muscles. Bone marrow-derived endothelial cells in the skeletal muscles slightly increased in number by physical training. No evidence of bone marrow-derived cardiac muscle nor skeletal muscle was present. There is a great difference in bone marrow derived cell type, and a great difference in organ distribution of bone marrow-derived endothelial cell number in the capillaries between the heart and skeletal muscles. Bone marrow-derived endothelial cells could be mobilized by physical training. Less
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