TNFalpha suppresses link protein and type II collagen expression in chondrocytes: Role of MEK1/2 and NF-kappaB signaling pathways.

Seguin CA; Bernier SM

首页> 外文期刊>Journal of Cellular Physiology >TNFalpha suppresses link protein and type II collagen expression in chondrocytes: Role of MEK1/2 and NF-kappaB signaling pathways.

【24h】

TNFalpha suppresses link protein and type II collagen expression in chondrocytes: Role of MEK1/2 and NF-kappaB signaling pathways.

机译：TNFalpha抑制蛋白质和II型的链接在软骨细胞胶原蛋白表达:角色MEK1/2 NF-kappaB信号通路。

获取原文

获取原文并翻译 | 示例

掌桥外文数据库（机构版） >>

开具论文收录证明 >>

文献代查 >>

页面导航

摘要
著录项
相似文献
相关主题

摘要

Tumor necrosis factor alpha (TNFalpha) inhibits matrix synthesis by chondrocytes in rheumatoid arthritis and osteoarthritis; however, the underlying signaling pathways are poorly characterized. This study investigated the TNFalpha-activated pathways regulating expression of two key components of the cartilage matrix-link protein and type II collagen. In rat articular chondrocytes, TNFalpha decreased link protein and type II collagen mRNA to undetectable levels within 48 h. Levels of link protein mRNA recovered more readily than type II collagen mRNA following removal of the cytokine. TNFalpha-mediated reduction in mRNA of both matrix molecules occurred at the level of transcription and, for link protein, mRNA stability. Turnover of type II collagen and link protein mRNA was dependent on new protein synthesis. In both prechondrocytes and articular chondrocytes, TNFalpha induced concentration-dependent activation of MEK1/2 and NF-kappaB, but not p38 or JNK. Sustained activation of NF-kappaB was observed for up to 72 h following continuous or transient exposure to TNFalpha. Using pharmacological and molecular approaches, the MEK1/2 and NF-kappaB pathways were found to mediate inhibition of type II collagen and link protein gene expression by TNFalpha. Both prechondrocytes and articular chondrocytes are targets of TNFalpha. This study identifies pathways through which TNFalpha perturbs the synthesis and organization of articular cartilage matrix during inflammation. J. Cell. Physiol. 197: 357-369, 2003Copyright 2003 Wiley-Liss, Inc.

机译：肿瘤坏死因子α(TNFalpha)抑制软骨细胞在类风湿性矩阵合成关节炎和骨关节炎;潜在的信号通路是差为特征。TNFalpha-activated通路调节表达两个关键组件的软骨matrix-link蛋白质和II型胶原蛋白。关节软骨细胞,TNFalpha减少链接蛋白质和II型胶原蛋白mRNA察觉在48 h水平。蛋白mRNA水平的链接恢复更容易比II型胶原蛋白mRNA删除后的细胞因子。减少TNFalpha-mediated mRNA矩阵发生在分子水平的信使rna转录,蛋白质链接稳定。蛋白mRNA依赖新的蛋白质合成。软骨细胞,TNFalpha诱导浓度激活MEK1/2和NF-kappaB,但不是p38或物。观察激活NF-kappaB长达72年h后连续的或短暂接触TNFalpha。方法,MEK1/2 NF-kappaB通路被发现调解抑制II型胶原蛋白基因表达和链接TNFalpha。软骨细胞是TNFalpha的目标。TNFalpha识别途径扰乱的合成和组织关节软骨基质在炎症。j .细胞。2003 Wiley-Liss, Inc。

著录项

来源
《Journal of Cellular Physiology》 |2003年第3期|356-369|共14页
作者
Seguin CA; Bernier SM;
展开▼
作者单位

CHIR Group in Skeletal Development and Remodeling, and Department of Anatomy and Cell Biology, The University of Western Ontario, London, Ontario, Canada.;

展开▼
收录信息
原文格式 PDF
正文语种英语
中图分类细胞生物学;
关键词
messengers; Chondrocyte; Cartilage MatrixCollagenAlternative NF-kappaB Signaling Pathwaylink proteinAtypical NF-kappaB Signaling PathwayCanonical NF-kappaB Signaling PathwayCollagen Type IITumor Necrosis Factor-alphaNF-kappa BRNA;

机译：messengers;Chondrocyte CartilageMatrixCollagenAlternative NF-kappaB信号Pathwaylink proteinAtypical NF-kappaB信号PathwayCanonical NF-kappaB信号PathwayCollagen类型IITumor坏死Factor-alphaNF-kappa BRNA;

相似文献

外文文献
中文文献

TNFalpha suppresses link protein and type II collagen expression in chondrocytes: Role of MEK1/2 and NF-kappaB signaling pathways.

摘要

著录项

相似文献

相关主题

期刊订阅