Liu Ruiyu, Liu Qi, Wang Kunzheng, Dang Xiaoqian, Zhang Feng
Department of Orthopedics, the Second Affiliated Hospital, Health Science Center, Xi'an Jiaotong University, Xi'an, Shaanxi, P.R. China.
Key Laboratory of Trace Elements and Endemic Diseases of National Health and Family Planning Commission, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an, Shaanxi, P. R. China.
Arthritis Res Ther. 2016 May 4;18(1):98. doi: 10.1186/s13075-016-0991-4.
The pathogenesis of necrosis of the femoral head (NFH) remains elusive. Limited studies were conducted to investigate the molecular mechanism of hip articular cartilage damage in NFH. We conducted genome-wide gene expression profiling of hip articular cartilage with NFH.
Hip articular cartilage specimens were collected from 18 NFH patients and 18 healthy controls. Gene expression profiling of NFH articular cartilage was carried out by Agilent Human 4x44K Gene Expression Microarray chip. Differently expressed genes were identified using the significance analysis of microarrays (SAM) software. Gene Ontology (GO) enrichment analysis of differently expressed genes was performed using the Database for Annotation, Visualization and Integrated Discovery (DAVID). Significantly differently expressed genes in the microarray experiment were selected for quantitative real-time PCR (qRT-PCR) and immunohistochemical validation.
SAM identified 27 differently expressed genes in NFH articular cartilage, functionally involved in extracellular matrix, cytokines, growth factors, cell cycle and apoptosis. The expression patterns of the nine validation genes in qRT-PCR were consistent with that in proteinaceous extracellular matrix (false discovery rate (FDR) = 3.22 × 10(-5)), extracellular matrix (FDR = 5.78 × 10(-5)), extracellular region part (FDR = 1.28 × 10(-4)), collagen (FDR = 3.22 × 10(-4)), extracellular region (FDR = 4.78 × 10(-4)) and platelet-derived growth factor binding (FDR = 5.23 × 10(-4)).
This study identified a set of differently expressed genes, implicated in articular cartilage damage in NFH. Our study results may provide novel insight into the pathogenesis and rationale of therapies for NFH.
股骨头坏死（NFH）的发病机制仍不清楚。针对NFH中髋关节软骨损伤的分子机制进行的研究有限。我们对NFH患者的髋关节软骨进行了全基因组基因表达谱分析。
收集18例NFH患者和18例健康对照者的髋关节软骨标本。采用安捷伦人类4x44K基因表达微阵列芯片对NFH关节软骨进行基因表达谱分析。使用微阵列显著性分析（SAM）软件鉴定差异表达基因。使用注释、可视化和综合发现数据库（DAVID）对差异表达基因进行基因本体（GO）富集分析。选择微阵列实验中显著差异表达的基因进行定量实时PCR（qRT-PCR）和免疫组化验证。
SAM鉴定出NFH关节软骨中有27个差异表达基因，其功能涉及细胞外基质、细胞因子、生长因子、细胞周期和细胞凋亡。qRT-PCR中9个验证基因的表达模式与蛋白质细胞外基质（错误发现率（FDR）=3.22×10⁻⁵）、细胞外基质（FDR=5.78×10⁻⁵）、细胞外区域部分（FDR=1.28×10⁻⁴）、胶原蛋白（FDR=3.22×10⁻⁴）、细胞外区域（FDR=4.78×10⁻⁴）和血小板衍生生长因子结合（FDR=5.23×10⁻⁴）中的表达模式一致。
本研究鉴定出一组与NFH关节软骨损伤相关的差异表达基因。我们的研究结果可能为NFH的发病机制和治疗原理提供新的见解。
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