Enhanced expression of insulin-like growth factor-binding proteins in human osteoarthritic cartilage detected by immunohistochemistry and in situ hybridization
Enhanced expression of insulin-like growth factor-binding proteins in human osteoarthritic cartilage detected by immunohistochemistry and in situ hybridization
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DOI：
10.1016/j.joca.2004.12.006
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发表时间：
2005-05-01
影响因子：
7
通讯作者：
Koji, T
中科院分区：
文献类型：
--
作者：
Iwanaga, H;Matsumoto, T;Koji, T
目的：探讨胰岛素样生长因子（IGF）和IGF结合蛋白（IGFBP）在骨关节炎（OA）发病机制中的作用。设计：CA患者股骨头软骨组织，股骨颈骨折患者作为对照。免疫组化和原位杂交检测IGFBP-3、-4和-5的表达，免疫组化检测IGF-I和IGF-I受体的表达。阳性软骨细胞的百分比是通过计算软骨表面、中间和深层区域的软骨细胞总数来确定的。结果：与对照软骨相比，所有igfbp中CA蛋白和信使RNA水平的阳性软骨细胞百分比明显增加。此外，igfbp和IGF-I/IGF-I受体的表达增强与软骨病变的组织学评分呈正相关。结论：骨性关节炎软骨组织中igfbp及IGF-I及其受体表达上调，提示igfbp参与了骨性关节炎的发病过程。(c) 2005年国际骨关节炎研究学会。Elsevier Ltd.出版。版权所有。
Objective: To determine the roles of insulin-like growth factor (IGF) and IGF-binding protein (IGFBP) in the pathogenesis of osteoarthritis (OA)Design: Cartilage tissues were obtained from the femoral heads of patients with CA, and those from patients with femoral neck fractures were used as a control. The expression of IGFBP-3, -4, and -5 was examined using immunohistochemistry and in situ hybridization, and IGF-I and IGF-I receptors were also immunohistochemically detected. The percentages of positive chondrocytes were determined by counting the total number of chondrocytes over the area of the surface, middle, and deep zones of the cartilage.Results: There was a marked increase in the percentage of positive chondrocytes in all IGFBPs on protein and messenger RNA levels for CA compared to that of the control cartilage. Furthermore, enhanced expression of IGFBPs and the IGF-I/IGF-I receptor was positively correlated with the histologic score for cartilage lesions.Conclusion: Up-regulation of IGFBPs as well as IGF-I and its receptor was observed for OA cartilage tissue, suggesting the involvement of IGFBPs in the pathogenesis of OA. (c) 2005 OsteoArthritis Research Society International. Published by Elsevier Ltd. All rights reserved.