Mechanism of the Development of Skin Sclerosis in Scleroderma
硬皮病皮肤硬化的发生机制
基本信息
- 批准号:12470176
- 负责人:
- 金额:$ 2.69万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (B)
- 财政年份:2000
- 资助国家:日本
- 起止时间:2000 至 2002
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
We previously established a mouse model for scleroderma by repeated local injections of bleomycin (J Invest Dermatol 1999 ; 112 : 456-462, J Rheumatol 1999 ; 26 : 2628-2634, Arch Dermatol Res 2000 ; 292 : 535-541). In this model, systemic treatment of interferon-γ reduced the development of dermal sclerosis (Arch Dermatol Res 2000 ; 292 : 362-365), whereas halofuginone was not effective (Rheumatology 2002 ; 41 : 594-596). Dermal sclerosis was also induced by bleomycin treatment in SCID mice, suggesting bleomycin-induced scleroderma is T cell independent (J Invest Dermatol 2001 ; 117 : 999-1001). Furthermore, expression of collagen was upregulated in mast cell-deficient mice (Arch Dermatol Res 2001 ; 293 : 532-536). Sclerotic fibroblasts following bleomycin treatment changed the phenotype into myofibroblasts, which were positive for α-smooth muscle actin (α-SMA), and neutralizing anti-TGF-β antibody decreased the number of α-SMA positive fibroblasts. Comparative study among various strains of mice revealed that increased expression and production of TGF-β in the lesional skin of bleomycin-'susceptible' strains.
用局部注射博来霉素建立硬皮病小鼠模型(J Invest Dermatol 1999; 112: 456-462; J Rheumatol 1999; 26: 2628-2634; Arch Dermatol 2000; 29: 535-541)。在这个模型中,干扰素-γ的全身治疗减少了皮肤硬化的发展(Arch Dermatol Res 2000; 292: 362-365),而halofuginone没有效果(Rheumatology 2002; 41: 594-596)。博来霉素治疗SCID小鼠也可诱导皮肤硬化,提示博来霉素诱导的硬皮病是T细胞不依赖的(J . Invest Dermatol 2001; 17: 99-1001)。此外,肥大细胞缺陷小鼠的胶原蛋白表达上调(Arch Dermatol Res 2001; 293: 532-536)。博来霉素处理后的硬化成纤维细胞表型转变为α-平滑肌肌动蛋白(α-SMA)阳性的肌成纤维细胞,中和抗tgf -β抗体可减少α-SMA阳性成纤维细胞的数量。不同品系小鼠的比较研究发现,博来霉素“敏感”品系病变皮肤中TGF-β的表达和产生增加。
项目成果
期刊论文数量(52)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Yamamoto T.&Nishioka K.: "Animal model of sclerotic skin : IV. Induction of dermal sclerosis by bleomycin is T cell independent"J Invest Dermatol. 117. 999-1001 (2001)
山本 T.
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Takagawa S, Lakos G, Mori Y, Yamamoto T, Nishioka K, Varga J.: "Sustained activation of fibroblast TGF- β/Smad signaling in murine scleroderma"J Invest Dermatol(accept).
Takakawa S、Lakos G、Mori Y、Yamamoto T、Nishioka K、Varga J.:“小鼠硬皮病中成纤维细胞 TGF-β/Smad 信号传导的持续激活”J Invest Dermatol(接受)。
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Yamamoto, T., Nishioka, K.: "Animal model of sclerotic skin : IV. Induction of dermal sclerosis by bleomycin is T cell independent"J Invest Dermatol.
Yamamoto, T.,Nishioka, K.:“硬化皮肤的动物模型:IV。博来霉素诱导真皮硬化是 T 细胞独立的”J Invest Dermatol。
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Yamamoto T., Nishioka K.: "Animal model of sclerotic skin. V : Increased expression of α-smooth muscle actin in fibroblastic cells in bleomycin-induced scleroderma"Clin Immunol. 102. 77-83 (2002)
Yamamoto T.,Nishioka K.:“硬化皮肤的动物模型。V:博莱霉素诱导的硬皮病中成纤维细胞中 α-平滑肌肌动蛋白的表达增加”Clin Nutritionol。
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Yamamoto T, et al.: "Mast cell-independent increase of type I collagen expression in experimental scleroderma induced by bleomycin"Arch Dermatol Res. 293. 532-536 (2001)
Yamamoto T 等人:“博来霉素诱导的实验性硬皮病中 I 型胶原蛋白表达的肥大细胞依赖性增加”Arch Dermatol Res。
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NISHIOKA Kiyoshi其他文献
NISHIOKA Kiyoshi的其他文献
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{{ truncateString('NISHIOKA Kiyoshi', 18)}}的其他基金
Analysis of Langerhans cell chemotactic factors
朗格汉斯细胞趋化因子分析
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07457189 - 财政年份:1996
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$ 2.69万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Analysis of the role of epidermal cytokines in skin inflammation
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63480246 - 财政年份:1988
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$ 2.69万 - 项目类别:
Grant-in-Aid for General Scientific Research (B)
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