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Genistein Inhibit Cytokines or Growth Factor-Induced Proliferation and Transformation Phenotype in Fibroblast-Like Synoviocytes of Rheumatoid Arthritis
Zhang, Yujun2; Dong, Jianqiang2; He, Peiying2; Li, Wende1,3; Zhang, Qi2; Li, Na2; Sun, Tiezheng1,3
关键词Rheumatoid Arthritis Fibroblast-like Synoviocyte Genistein Transformation
刊名INFLAMMATION
2012-02-01
DOI10.1007/s10753-011-9365-x
35期:1页:377-387
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Cell Biology ; Immunology
研究领域[WOS]Cell Biology ; Immunology
关键词[WOS]BREAST-CANCER CELLS ; SYNOVIAL FIBROBLASTS ; JOINT DESTRUCTION ; FACTOR-BETA ; IN-VITRO ; EXPRESSION ; APOPTOSIS ; KINASE ; METALLOPROTEINASE ; COLLAGENASE
英文摘要

The purpose of this research is to study the effect of genistein on cytokines or growth factor-induced proliferation and transformation phenotype of rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS). RA-FLS were primarily cultured. With respective stimulation of IL-1 beta, TNF-alpha, and EGF, genistein was applied to elucidate its effect on synoviocytes′ growth number, cell proliferation assay, cell cycle using cell counts, H-3-TdR incorporation and flow cytometry, the colony numbers under anchorage-independent condition, and the expression of MMP-2 and MMP-9 in synovial fibroblasts. EGF, IL-1 beta, and TNF-alpha increased H-3 incorporation in RA-FLS, respectively. EGF augmented clone numbers of RA-FLS under anchorage-independent condition and not IL-1 beta and TNF-alpha. Genistein had an inhibitory role on cell number and H-3-TdR incorporation of RA-FLS stimulated with IL-1 beta, TNF-alpha and EGF; genistein arrested the cell cycle at G(1) restriction point; genistein decreased colony numbers under anchorage-independent condition stimulated by EGF in serum condition. IL-1 beta or TNF-alpha increased expression of MMP-9 and MMP-2 in rheumatoid synoviocytes; EGF stimulated expression of MMP-9 but not of MMP-2; genistein suppressed production of MMP-9 more than MMP-2 induced by IL-1 beta or TNF-alpha; rMMP-9, rMMP-2, or their inhibitors had no effect on the H-3-TdR incorporation of synovial cells. Erk1/2 inhibitor (PD098 059) had obvious inhibitory effect on the H-3 incorporation induced by TNF-alpha or IL-1 beta; inhibitors of JNK (SP600 125) had no significant effect on the H-3 incorporation. While pretreatment with PD098059 had no marked inhibitory effect on MMP-9 expression induced by TNF-alpha or IL-1 beta, SP600125 decreased significantly the MMP-9 expression induced by TNF-alpha or IL-1 beta. Neither PD098059 nor SP600 125 could inhibit the MMP-2 expression induced by TNF-alpha or IL-1 beta. Genistein inhibited IL-1 beta, TNF-alpha or EGF-induced proliferation and MMP-9 expression in fibroblast-like synoviocytes of rheumatoid arthritis; the proliferation of RA-FLS was mediated by Erk1/2 but not JNK activation, while JNK activation was involved in the signal transduction pathway leading to MMP-9 expression in rheumatoid synoviocytes.

语种英语
WOS记录号WOS:000300550900043
项目编号30801160
资助机构National Natural Science Foundation of China
引用统计
被引频次:25[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/56192
专题北京大学第二临床医学院
北京大学第二临床医学院_中心实验室
作者单位1.Peking Univ, Arthrit Clin, Beijing 100044, Peoples R China
2.Peking Univ, Peoples Hosp, Clin Inst Mol Biol, Beijing 100044, Peoples R China
3.Peking Univ, Peoples Hosp, Res Ctr, Beijing 100044, Peoples R China
推荐引用方式
GB/T 7714
Zhang, Yujun,Dong, Jianqiang,He, Peiying,et al. Genistein Inhibit Cytokines or Growth Factor-Induced Proliferation and Transformation Phenotype in Fibroblast-Like Synoviocytes of Rheumatoid Arthritis[J]. INFLAMMATION,2012,35(1):377-387.
APA Zhang, Yujun.,Dong, Jianqiang.,He, Peiying.,Li, Wende.,Zhang, Qi.,...&Sun, Tiezheng.(2012).Genistein Inhibit Cytokines or Growth Factor-Induced Proliferation and Transformation Phenotype in Fibroblast-Like Synoviocytes of Rheumatoid Arthritis.INFLAMMATION,35(1),377-387.
MLA Zhang, Yujun,et al."Genistein Inhibit Cytokines or Growth Factor-Induced Proliferation and Transformation Phenotype in Fibroblast-Like Synoviocytes of Rheumatoid Arthritis".INFLAMMATION 35.1(2012):377-387.
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