Regulation of gelatinases expression by cytokines, endotoxin, and pharmacological agents in the human osteoarthritic knee.

doi:10.1080/03008200490506058

中山醫學大學機構典藏 CSMUIR > 醫學院 > 醫學系 > 期刊論文 > Item 310902500/10541

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题名:	Regulation of gelatinases expression by cytokines, endotoxin, and pharmacological agents in the human osteoarthritic knee.
作者:	Chu, SC Yang, SF Lue, KH Hsieh, YS Wu, CL Lu, KH
贡献者:	中山醫學大學
关键词:	Cytokine;Endotoxin;MMP-2;MMP-9;Osteoarthritis;Pharmacological Agent
日期:	2004
上传时间:	2015-03-23T05:09:40Z (UTC)
ISSN:	0300-8207
摘要:	We examined the amount of gelatinases (matrix metalloproteinase-2 and -9 [MMP-2 and MMP-9] in a series of chondral, meniscal, and synovial cultures of early osteoarthritis (OA) after treatment with or without catabolic cytokines. These included interleukin-1alpha (IL-1alpha) and tumor necrosis factor-alpha (TNF-alpha), lipopolysaccharide (LPS), and pharmacological agents, including plasmin/serine proteinase antagonist aprotinin, protein synthesis inhibitor cycloheximide, and protein kinase C (PKC) inhibitors staurosporine, H7, and Gö6976 for investigation of their effects on MMP-2 and -9 production in OA. Gelatin zymography revealed that IL-alpha, TNF-alpha, and LPS could elevate MMP-2 secretion in all tissue cultures and also increase MMP-9 production in all synovial and some meniscal cultures. In contrast, aprotinin, cycloheximide, staurosporine, H7, and Gö6976 could suppress MMP-2 secretion in all tissue cultures and also decrease MMP-9 production in all synovial and some meniscal cultures. Our data indicate that catabolic cytokines and LPS may promote tissue destruction and disintegration of extracellular matrix in early OA. Agents that target on the PKC pathway, plasmin/serine proteinase or protein synthesis for MMP-2 and -9 in early OA may inhibit the production of MMPs. These findings might contribute to the design of more efficacious therapies.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/10541 http://dx.doi.org/10.1080/03008200490506058
關聯:	Connect Tissue Res. 2004;45(3):142-50.
显示于类别:	[醫學系] 期刊論文

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