Expression profiles of genes involved in apoptosis and selenium metabolism in articular cartilage of patients with Kashin-Beck osteoarthritis

Expression profiles of genes involved in apoptosis and selenium metabolism in articular cartilage of patients with Kashin-Beck osteoarthritis
复制标题

DOI:
10.1016/j.gene.2013.11.050
复制
发表时间:
2014-02-10
期刊:
影响因子:
3.5
通讯作者:
Guo, Xiong
Guo, Xiong
中科院分区:
生物学3区
文献类型:
--
作者:
Wu, Shi-Xun;Wang, Wei-Zhuo;Guo, Xiong

文献摘要

被引文献

相似文献

大骨节病是一种特殊类型的地方性骨关节炎。研究表明硒代谢和细胞凋亡的改变在大骨节病中起一定作用。然而,其潜在的分子机制仍不清楚。我们使用从大骨节病患者和健康对照的软骨中分离的RNA,通过微阵列显著性分析(SAM)软件进行微阵列分析。通过不相容性通路分析(IPA)和枢纽基因分析,研究了功能基因网络和差异表达基因相关的关键分子。实时荧光定量PCR检测芯片检测的有效性。我们在大骨节病组和对照组中发现了52个上调的凋亡相关基因和26个下调的硒相关基因,这些基因与MYC介导的凋亡信号通路有关。我们用定量实时PCR分析证实了阵列研究的结果。我们的研究结果表明,通过MYC介导的信号通路对硒代谢和细胞凋亡的异常调节参与了大骨节病的发病,但未发现凋亡基因与硒基因之间的关系。(C)2013 Elsevier B.V.版权所有。
Kashin-Beck disease (KBD) is a special type of endemic osteoarthritis. It has been suggested that alterations in selenium metabolism and apoptosis play a role in KBD. However, the underlying molecular mechanism remains largely unclear. We performed a microarray analysis using RNA isolated from cartilages of KBD patients and healthy controls, through Significance Analysis of Microarray (SAM) software. Functional gene networks and crucial molecules associated with differentially expressed genes were investigated via Ingenuity Pathway Analysis (IPA) and hub gene analysis. Quantitative real-time PCR was used to check the validation of chip test. We identified 52 up-regulated apoptosis-related genes and 26 down-regulated selenium-related genes between KBD and controls, and these genes associated with the "MYC-mediated apoptosis signaling pathway". We confirmed the results from array studies with quantitative real-time PCR analysis. Our results suggest that abnormal regulation of selenium metabolism and apoptosis through the MYC mediated signaling pathway contributes to the pathogenesis of KBD, but the relationship between apoptosis gene and selenium gene was not found. (C) 2013 Elsevier B.V. All rights reserved.