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Microarray study of gene expression profile to identify new candidate genes involved in the molecular mechanism of leptin-induced knee joint osteoarthritis in rat

机译:基因表达谱的微阵列研究,以鉴定参与瘦素诱导的大鼠膝关节骨关节炎分子机制的新候选基因

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Osteoarthritis (OA) is one of the most prevalent chronic joint diseases while the precise genetic mechanism remains elusive. In this study, we investigated the gene expression profile in OA by microarray analysis. Histopathological characteristics of OA cartilage were examined using a rat model of leptin-induced OA. Gene expression profile of leptin-induced articular cartilage and healthy rat cartilage were compared using genome-wide microarray hybridization. A total of 1857 genes differentially expressed genes (1197 upregulated and 660 downregulated) were identified, some of which are known to be associated with leptin-induced OA phenotype. These included genes related to MMPs, inflammatory factors, growth factors, apoptotic genes and osteogenic genes. In addition, upregulated expressions of some new candidate genes, which have hitherto fore not been linked to OA (such as BCL2L11) were detected in leptin-induced OA cartilage, which suggests that these genes might be important for OA molecular mechanism. Our findings suggest that pathogenesis of leptin-induced OA involves modulation of expression of multiple genes, although the underlying molecular mechanisms need to be studied further. Further investigation of leptin-induced gene expression changes is needed to gain new insights into the molecular mechanism of OA pathogenesis.
机译:骨关节炎(OA)是最流行的慢性关节疾病之一,而确切的遗传机制仍然难以捉摸。在这项研究中,我们通过微阵列分析调查了OA中的基因表达谱。使用瘦蛋白诱导的OA大鼠模型检查了OA软骨的组织病理学特征。使用全基因组微阵列杂交比较了瘦素诱导的关节软骨和健康大鼠软骨的基因表达谱。共鉴定出1857个差异表达基因(上调1197个基因,下调660个基因),其中一些已知与瘦素诱导的OA表型有关。这些包括与MMP,炎性因子,生长因子,凋亡基因和成骨基因有关的基因。此外,在瘦素诱导的OA软骨中检测到一些迄今尚未与OA相关的新候选基因的表达上调,这表明这些基因可能对OA分子机制很重要。我们的发现表明,尽管潜在的分子机制需要进一步研究,但瘦素诱导的OA的发病机制涉及多个基因表达的调节。需要进一步研究瘦蛋白诱导的基因表达变化,以获得对OA发病机理的分子机制的新见解。

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