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Role of Chemokines in the Pathogenesis of Bleomycin-induced Scleroderma

Role of Chemokines in the Pathogenesis of Bleomycin-induced Scleroderma
趋化因子在博来霉素诱导的硬皮病发病机制中的作用
批准号:
12670810
负责人:
YAMAMOTO Toshiyuki
金额:
$2.3万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2000
资助国家:
日本
项目状态:
已结题
起止时间:
2000 至 2002

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项目成果

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中文摘要
翻译
最近的研究结果表明,趋化因子参与了纤维化过程。我们报道了MCP-1不仅上调胶原蛋白的mRNA表达,而且上调胶原酶和金属蛋白酶-1组织抑制剂(TIMP-1)的mRNA表达(J immunojournal; 2000; 164: 6174-6179)。MCP-1在系统性硬化症(SSc)病变皮肤中被强烈检测到(J Dermatol Sci 2001; 26: 133-139), MCP-1的自发mRNA表达在硬皮病成纤维细胞中也升高(Eur J Immunol 2001; 31: 2936-2941)。我们先前通过反复注射博来霉素建立了小鼠硬皮病模型,从组织学和生化角度模拟人类硬皮病(J Invest Dermatol 1999; 112: 456-462; J Rheumatol 1999; 26: 2628-2634; Arch Dermatol 2000; 292: 535-541)。在该模型中,博来霉素治疗后,MCP-1及其受体CCR-2在病变皮肤中的表达增强,体内抗MCP-1抗体中和和局部博来霉素治疗减少了真皮硬化的发展。体外数据显示MCP-1上调细胞外基质蛋白mRNA的表达。这些数据提示MCP-1/CCR-2通路在博莱霉素诱导的硬皮病发病机制中起重要作用。
英文摘要
Recent findings suggest the involvement of chemokines in the fibrotic process. We reported that MCP-1 upregulates mRNA expression of not only collagen, but also collagenase and tissue inhibitor of metalloproteinase-1 (TIMP-1) (J Immunol 2000; 164: 6174-6179). MCP-1 was strongly detected in the lesional skin of systemic sclerosis (SSc) (J Dermatol Sci 2001; 26: 133-139), and spontaneous mRNA expression of MCP-1 was also elevated in scleroderma fibroblasts (Eur J Immunol 2001; 31: 2936-2941). We previously established a mouse model for scleroderma by repeated injections of bleomycin, mimicking human scleroderma both histologically and biochemically (J Invest Dermatol 1999; 112: 456-462, J Rheumatol 1999; 26: 2628-2634, Arch Dermatol Res 2000; 292: 535-541). In this model, expression of MCP-1 as well as its receptor, CCR-2, was enhanced in the lesional skin following bleomycin treatment, in vivo neutralization with anti-MCP-1 antibody together with local bleomycin treatment reduced the development of dermal sclerosis. In vitro data demonstrated that MCP-1 upregulates mRNA expression of extracellular matrix proteins. These data suggest MCP-1/CCR-2 pathway plays an important role in the pathogenesis of bleomycin-induced scleroderma.
期刊论文(27)
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会议论文
Yamamoto T, et al.: "Monocyte chemoattractant protein-1 enhances gene expression and synthesis of matrix metalloproteinase-1 in human fibroblasts by an autocrine IL-1 α loop"J Immunol. 164. 6174-6179 (2000)
Yamamoto T 等人:“单核细胞趋化蛋白 1 通过自分泌 IL-1 α 环增强人成纤维细胞中基质金属蛋白酶 1 的基因表达和合成”J 免疫学杂志 164. 6174-6179 (2000)
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通讯作者:
Yamamoto, T.: "Animal model of sclerotic skin induced by bleomycin : A Clue to the pathogenesis of and therapy for scleroderma?"Clin Immunol. 102. 209-216 (2002)
Yamamoto, T.:“博来霉素诱导的硬化皮肤动物模型:硬皮病发病机制和治疗的线索?”Clin Nutrition。
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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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通讯作者:
Yamamoto T, et al.: "High expression and autoinduction of monocyte chemoattractant protein-1 in scleroderma fibroblasts"Eur J Immunol.. 31. 2936-2941 (2001)
Yamamoto T 等人:“硬皮病成纤维细胞中单核细胞趋化蛋白-1 的高表达和自诱导”Eur J Nutrition.. 31. 2936-2941 (2001)
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