前交叉韧带离断联合半月板切除诱发的骨关节炎早期模型相关基因芯片数据的生物信息学分析

发布时间：2018-05-20 19:32

本文选题：骨关节炎 + 差异表达基因　；参考：《中国运动医学杂志》2017年09期

【摘要】：目的:探讨前交叉韧带(anterior cruciate ligament,ACL)离断联合半月板切除诱发的骨关节炎(osteoarthritis,OA)的基因表达和生物过程的改变,为OA分子机制的进一步研究提供生物信息学依据。方法:从GEO数据库下载Appleton等构建的ACL离断联合半月板切除诱发的OA早期大鼠模型的基因芯片数据集,应用生物信息学方法筛选差异表达基因(differentially expressed genes,DEGs),并进行基因本体论(Gene ontology,GO)和日本京都基因和基因组百科全书代谢通路数据库(Kyoto Encyclopedia of Genes and Genomes,KEGG)通路富集分析。结果:共筛选出170个DEGs,其中包括97个上调基因和73个下调基因。上调基因主要富集在细胞外基质,并与细胞外基质交互通路等信号通路关系密切。而下调基因主要富集在肌肉收缩的生物学功能中,并与PPAR通路等信号通路关系密切。结论:细胞外基质和肌肉收缩的改变对OA的发生发展起着关键作用。细胞外基质受体交互通路和PPAR信号通路与OA密切相关,值得进一步深入研究。
[Abstract]:Objective: to investigate the gene expression and biological process of osteoarthritis induced by anterior cruciate ligament amputation combined with meniscectomy, and to provide bioinformatics basis for further study on the molecular mechanism of OA. Methods: the gene-chip data set of the early OA rat model induced by ACL disconnection and meniscectomy was obtained by downloading Appleton from GEO database. Bioinformatics method was used to screen differentially expressed genes (expressed genesus) and to analyze the enrichment of gene ontology (GOG) and Kyoto Encyclopedia of Genes and genomes (KEGG) pathway in Kyoto gene and genome encyclopedia of Japan. Results: 170 DEGs were screened, including 97 up-regulated genes and 73 down-regulated genes. The up-regulated genes are mainly concentrated in extracellular matrix and are closely related to signal pathways such as extracellular matrix interaction pathway. The down-regulated genes are mainly concentrated in the biological function of muscle contraction and are closely related to signal pathways such as PPAR pathway. Conclusion: the changes of extracellular matrix and muscle contraction play a key role in the development of OA. Extracellular matrix receptor interaction pathway and PPAR signaling pathway are closely related to OA.
【作者单位】：复旦大学附属华山医院运动医学科;
【基金】：国家高技术研究发展计划(863计划)(2015AA033703) 国家自然科学基金(81572108,81370052) 国家重点研发计划项目(2016YFC1100300)
【分类号】：R684.3

【相似文献】