Involvement of the TGF-.BETA.1 Derived from Megakaryocyte in the PEG-rHuMGDF-Induced Myelofibrosis and Bone Formation.
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- Ide Youichi
- Pharmaceutical Development Laboratories, Kirin Brewery Co., Ltd.
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- Yamanaka Eri
- Pharmaceutical Development Laboratories, Kirin Brewery Co., Ltd.
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- Namiki Yasuko
- Pharmaceutical Development Laboratories, Kirin Brewery Co., Ltd.
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- Iijima Rieko
- Pharmaceutical Development Laboratories, Kirin Brewery Co., Ltd.
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- Harada Katsuhiko
- Pharmaceutical Development Laboratories, Kirin Brewery Co., Ltd.
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- Ishi Hiromi
- Pharmaceutical Development Laboratories, Kirin Brewery Co., Ltd.
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- Kawahara Jun-ichi
- Pharmaceutical Development Laboratories, Kirin Brewery Co., Ltd.
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- Doi Kunio
- Department of Veterinary Pathology, Faculty of Agriculture, The University of Tokyo
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抄録
Bone marrow fibrosis and new bone formation were induced by Pegylated recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF) injection in the rat. We investigated time course changes of megakaryocyte counts, circulating platelet counts, transforming growth factor-β1 (TGF-β1) levels in the bone marrow and those in platelet-poor plasma (PPP) when rats were injected with PEG-rHuMGDF at a dose of 0.1 mg/kg. Additionally, ultrastructural analysis of the circulating platelet and the bone marrow was performed by electron microscope. PEG-rHuMGDF injection daily for 5 days caused a megakaryocyte hyperplasia on days 5-7[after the commencement of the treatment], myelofibrosis on days 7-10, and new bone formation on days 8-15. TGF-β1 levels in the extracellular fluid of the marrow, megakaryocyte numbers, TGF-β1 levels in the PPP, and circulating platelet counts increased by PEG-rHuMGDF injection, and reached to the maximum level on days 7, 7, 8, and 10, respectively. Ultrastructural analysis showed that circulating platelets had no prominent morphological changes in the PEG-rHuMGDF-treated rats on day 8, compared with vehicle-treated rats. Additionally, there were many platelets or fragments of megakaryocyte around mesenchymal cells, and those fragments deposited in the newly formed bone on day 10. These data suggested that myelofibrosis and new bone formation were induced by the increase of TGF-β1 levels derived from bone marrow megakaryocytes.
収録刊行物
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- Journal of Toxicologic Pathology
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Journal of Toxicologic Pathology 15 (1), 31-38, 2002
日本毒性病理学会
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詳細情報 詳細情報について
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- CRID
- 1390001204416263552
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- NII論文ID
- 10020559768
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- NII書誌ID
- AA12022786
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- COI
- 1:CAS:528:DC%2BD38XjtFOgs74%3D
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- ISSN
- 1881915X
- 09149198
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
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- 使用不可