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学科主题: 口腔医学
题名:
Role of Wnt-5A in Interleukin-1 beta-Induced Matrix Metalloproteinase Expression in Rabbit Temporomandibular Joint Condylar Chondrocytes
作者: Ge, Xianpeng2; Ma, Xuchen1,2; Meng, Juanhong2; Zhang, Chenguang3; Ma, Kangtao3; Zhou, Chunyan3
刊名: ARTHRITIS AND RHEUMATISM
发表日期: 2009-09-01
DOI: 10.1002/art.24779
卷: 60, 期:9, 页:2714-2722
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Rheumatology
研究领域[WOS]: Rheumatology
关键词[WOS]: N-TERMINAL KINASE ; CELLS IN-VITRO ; RHEUMATOID-ARTHRITIS ; ARTICULAR CHONDROCYTES ; GENE-EXPRESSION ; KAPPA-B ; DIFFERENTIAL REGULATION ; CARTILAGE DESTRUCTION ; SIGNALING PATHWAYS ; PROTEIN-KINASES
英文摘要:

Objective. To determine the possible involvement and regulatory mechanisms of Wnt-5A signaling in interleukin-1 beta (IL-1 beta)-induced increase in matrix metalloproteinase 1 (MMP-1), MMP-3, MMP-9, and MMP-13 expression in temporomandibular joint (TMJ) condylar chondrocytes.

Methods. Primary rabbit condylar chondrocytes were treated with IL-1 beta, purified Wnt-5A protein, or both and transfected with Wnt-5A expression vector. Expression of Wnt-5A, MMP-1, MMP-3, MMP-9, MMP-13, and type II collagen, as well as cell morphologic changes, were examined. To explore the mechanisms of action of Wnt-5A, the accumulation and nuclear translocation of beta-catenin, the transcription activity of the beta-catenin-Tcf/Lef complex, phosphorylated JNK, phosphorylated ERK, and phosphorylated p38 were analyzed. SP600125, a JNK inhibitor, was used to investigate the role of the JNK pathway in Wnt-5A induction of MMP-1, MMP-3, MMP-9, and MMP-13.

Results. Treatment of rabbit condylar chondrocytes with IL-1 beta up-regulated Wnt-5A expression. Purified Wnt-5A protein and transfection with Wnt-5A expression vector promoted the expression of MMP-1, MMP-3, MMP-9, and MMP-13. Wnt-5A did not cause accumulation and nuclear translocation of beta-catenin or activation of the beta-catenin-Tcf/Lef transcription complex. Instead, Wnt-5A activated JNK, and an inhibitor of JNK blocked the Wnt-5A-induced up-regulated expression of MMPs.

Conclusion. These findings indicate that IL-1 beta up-regulates Wnt-5A, and the activation of Wnt-5A signaling induces the expression of MMP-1, MMP-3, MMP-9, and MMP-13 via the JNK signaling pathway in rabbit TMJ condylar chondrocytes. Blockage of JNK signaling impairs the Wnt-5A-induced up-regulation of MMPs. Thus, Wnt-5A may be associated with cartilage destruction by promoting the expression of MMPs.

语种: 英语
所属项目编号: 30772439
项目资助者: National Natural Science Foundation of China
WOS记录号: WOS:000270054900021
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/56269
Appears in Collections:北京大学口腔医学院_期刊论文

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作者单位: 1.Peking Univ, Sch Stomatol, Beijing 100081, Peoples R China
2.Peking Univ, Sch Basic Med Sci, Beijing 100081, Peoples R China
3.Peking Univ, Hosp Stomatol, Ctr Temporomandibular Disorders & Orofacial Pain, Beijing 100081, Peoples R China

Recommended Citation:
Ge, Xianpeng,Ma, Xuchen,Meng, Juanhong,et al. Role of Wnt-5A in Interleukin-1 beta-Induced Matrix Metalloproteinase Expression in Rabbit Temporomandibular Joint Condylar Chondrocytes[J]. ARTHRITIS AND RHEUMATISM,2009,60(9):2714-2722.
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