中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/34974
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    题名: Intra-articular lentivirus-mediated delivery of galectin-3 shRNA and galectin-1 gene ameliorates collagen-induced arthritis.
    作者: (Wang CR);(Shiau AL);(Chen SY);(Cheng ZS);(Li YT);李哲欣(Lee, Che-Hsin);(Yo YT);(Lo CW);(Lin YS);(Juan HY);(Chen YL);(Wu CL)*
    贡献者: 醫學系
    关键词: galectin-3;galectin-1;collagen-induced arthritis;T-cell death;angiogenesis;rheumatoid arthritis
    日期: 2010-10
    上传时间: 2010-11-24 16:05:09 (UTC+8)
    摘要: Different members of the galectin family may have inhibitory
    or stimulatory roles in controlling immune responses and
    regulating inflammatory reactions in autoimmune diseases
    such as rheumatoid arthritis (RA). A hypothetical model of a
    cross talk between galectin-1 and galectin-3 has been
    established in the circumstance of rheumatoid joints. As
    galectin-3 is a positive regulator and galectin-1 is a negative
    regulator of inflammation and autoimmune responses, in this
    study we evaluated the effects of local knockdown of
    galectin-3 or overexpression of galectin-1 on ameliorating
    collagen-induced arthritis (CIA) in rats. Lentiviral vectors
    encoding galectin-3 small hairpin RNA (shRNA) and
    galectin-1, as well as two control vectors expressing
    luciferase shRNA and green fluorescent protein, were
    individually injected intra-articularly into the ankle joints of
    rats with CIA, and their treatment responses were monitored
    by measuring the clinical, radiological and histological
    changes. Our results show that both knockdown of galectin-
    3 and overexpression of galectin-1 induced higher
    percentages of antigen-induced T-cell death in the lymph
    node cells from arthritic rats. Furthermore, these treatments
    significantly reduced articular index scores, radiographic
    scores and histological scores, accompanied with decreased
    T-cell infiltrates and reduced microvessel density in the ankle
    joints. Our findings implicate galectin-3 and galectin-1 as
    potential therapeutic targets for the treatment of RA.
    關聯: GENE THERAPY 17(10):1225-1233
    显示于类别:[醫學系] 期刊論文

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