Screening of differentially expressed genes associated with non-union skeletal fractures and analysis with a DNA microarray

被引:7
作者
Xu, Jiaming [1 ]
Zhang, Changqing [1 ]
Song, Wenqi [1 ]
机构
[1] Shanghai Jiao Tong Univ, Dept Orthoped, Shanghai Peoples Hosp 6, Shanghai 200233, Peoples R China
基金
中国国家自然科学基金;
关键词
non-union skeletal fractures; differentially expressed gene; interaction network; function enrichment analysis; pathway analysis; UBIQUITIN LIGASE; CELL; P53; MDM2; DEGRADATION; RESPONSES; PATHWAY; CANCER;
D O I
10.3892/etm.2014.1478
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The purpose of this study was to identify the feature genes that are associated with non-union skeletal fractures using samples of normal union and non-union skeletal fracture microarray data. The gene expression profile GSE494 was downloaded from the Gene Expression Omnibus database and included 12 samples based on three different platforms (GPL92, GPL93 and GPL8300). Each of the platforms had four sets of expression data, two from normal union skeletal fracture samples and two from non-union skeletal fracture samples. The differentially expressed genes within the three platforms of expression data were identified using packages in R language and the differentially expressed genes common to the three platforms were selected. The selected common differentially expressed genes were further analyzed using bioinformatic methods. The software HitPredict was used to search interactions of the common differentially expressed genes and then FuncAssociate was used to conduct a functional analysis of the genes in the interaction network. Further, the associated pathways were identified using the software WebGestalt. Under the three different platforms, GPL92, GPL93 and GPL8300, the numbers of differentially expressed genes identified were 531, 418 and 914, respectively. The common gene CLU and its interacting genes were most significantly associated with the regulation of sterol transport and the osteoclast differentiation pathway. Upregulation of the gene CLU was identified by comparing data for normal union and non-union skeletal fracture samples. According to the function of CLU and its interacting genes, it was concluded that they inhibit the normal healing process following a fracture, and result in non-union skeletal fractures through the regulation of sterol transport and the pathways of differentiation in osteoclasts.
引用
收藏
页码:609 / 614
页数:6
相关论文
共 39 条
[1]   Molecular mechanisms controlling bone formation during fracture healing and distraction osteogenesis [J].
Ai-Aql, Z. S. ;
Alagl, A. S. ;
Graves, D. T. ;
Gerstenfeld, L. C. ;
Einhorn, T. A. .
JOURNAL OF DENTAL RESEARCH, 2008, 87 (02) :107-118
[2]   Synoviolin/Hrd1, an E3 ubiquitin ligase, as a novel pathogenic factor for arthropathy [J].
Amano, T ;
Yamasaki, S ;
Yagishita, N ;
Tsuchimochi, K ;
Shin, H ;
Kawahara, K ;
Aratani, S ;
Fujita, H ;
Zhang, L ;
Ikeda, R ;
Fujii, R ;
Miura, N ;
Komiya, S ;
Nishioka, K ;
Maruyama, I ;
Fukamizu, A ;
Nakajima, T .
GENES & DEVELOPMENT, 2003, 17 (19) :2436-2449
[3]  
[Anonymous], 2008, ARTHR REL COND US BO, P99
[4]  
Assmann G, 2009, CLIN EXP RHEUMATOL, V27, P615
[5]   Next generation software for functional trend analysis [J].
Berriz, Gabriel F. ;
Beaver, John E. ;
Cenik, Can ;
Tasan, Murat ;
Roth, Frederick P. .
BIOINFORMATICS, 2009, 25 (22) :3043-3044
[6]   A single nucleotide polymorphism in the MDM2 promoter attenuates the p53 tumor suppressor pathway and accelerates tumor formation in humans [J].
Bond, GL ;
Hu, WW ;
Bond, EE ;
Robins, H ;
Lutzker, SG ;
Arva, NC ;
Bargonetti, J ;
Bartel, F ;
Taubert, H ;
Wuerl, P ;
Onel, K ;
Yip, L ;
Hwang, SJ ;
Strong, LC ;
Lozano, G ;
Levine, AJ .
CELL, 2004, 119 (05) :591-602
[7]   MOLECULAR ANALYSIS AND CHROMOSOMAL MAPPING OF AMPLIFIED GENES ISOLATED FROM A TRANSFORMED MOUSE 3T3-CELL LINE [J].
CAHILLYSNYDER, L ;
YANGFENG, T ;
FRANCKE, U ;
GEORGE, DL .
SOMATIC CELL AND MOLECULAR GENETICS, 1987, 13 (03) :235-244
[8]   The tumour-suppressive function of CLU is explained by its localisation and interaction with HSP60 [J].
Chaiwatanasirikul, K-A ;
Sala, A. .
CELL DEATH & DISEASE, 2011, 2 :e219-e219
[9]  
Cleveland KB, 1987, CAMPBELLS OPERATIVE, P2053
[10]   High throughput proteomic analysis of the secretome in an explant model of articular cartilage inflammation [J].
Clutterbuck, Abigail L. ;
Smith, Julia R. ;
Allaway, David ;
Harris, Pat ;
Liddell, Susan ;
Mobasheri, Ali .
JOURNAL OF PROTEOMICS, 2011, 74 (05) :704-715