Advanced glycation end products increases matrix metalloproteinase-1, -3, and -13, and TNF-α in human osteoarthritic chondrocytes
Advanced glycation end products increases matrix metalloproteinase-1, -3, and -13, and TNF-α in human osteoarthritic chondrocytes
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DOI：
10.1016/j.febslet.2007.03.090
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发表时间：
2007-05-01
期刊：
影响因子：
3.5
通讯作者：
Lee, Chang-Keun
中科院分区：
文献类型：
--
作者：
Nah, Seong-Su;Choi, In-Young;Lee, Chang-Keun
我们研究了晚期糖基化终末产物（AGE）的作用，它随着年龄的增长在人骨关节炎软骨细胞的关节软骨中积累。我们发现AGE-BSA以剂量依赖性方式显著增加MMP-1、-3和-13和TNF-α。AGE-BSA刺激的JNK、p38、ERK和NF-κ B活性。AGE-BSA对MMP-1、-3和-13的刺激作用可被特异性JNK、p38抑制剂逆转，表明JNK和p38参与AGE-BSA诱导的MMP和TNF-α。我们还观察到NF-κ B B参与AGE-BSA诱导的TNF-α。用可溶性AGE受体（sNAG）预处理也减少了AGE刺激的MMPs和TNF-α，暗示AGE受体（sNAG）的参与。总之，AGE的积累可能通过增加MMP-1、MMP-3和MMP-13以及TNF-α在骨关节炎的发展中发挥作用。(c)2007年欧洲生物化学学会联合会。Elsevier B. V.出版，保留所有权利。
We investigated the effects of advanced glycation end products (AGE) which accumulate in articular cartilage with age in human osteoarthritic chondrocytes. We found AGE-BSA significantly increased MMP-1, -3, and -13, and TNF-alpha in a dose-dependent manner. AGE-BSA-stimulated JNK, p38, and ERK and NF-kappa B activity. The stimulatory effect of AGE-BSA on MMP-1, -3, and -13 were reversed by treatment with specific JNK, p38 inhibitors, suggesting JNK and p38 are involved in AGE-BSA-induced MMPs and TNF-alpha. We also observed that NF-kappa B is involved in AGE-BSA-induced TNF-alpha. Pretreatment with soluble receptor for AGE (sRAGE) also reduced AGE-stimulated MMPs and TNF-alpha, implicating the involvement of receptor for AGE (RAGE). In conclusion, accumulation of AGE may have a role in the development of osteoarthritis by increasing MMP-1, -3, and -13, and TNF-alpha. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.