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

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS ACS Applied Bio Materials Pub Date : 2017-07-04 eCollection Date: 2018-01-01 DOI:10.1186/s41065-017-0039-z
Qing Fan, Zhu Liu, Chao Shen, Hai Li, Jing Ding, Fangchun Jin, Lin Sha, Ziming Zhang
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引用次数: 10

Abstract

Background: 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.

Results: 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.

Conclusion: 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.

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基因表达谱的微阵列研究,以确定参与瘦素诱导大鼠膝关节骨关节炎分子机制的新候选基因。
背景:骨关节炎(OA)是最常见的慢性关节疾病之一,其确切的遗传机制尚不清楚。在这项研究中,我们通过微阵列分析研究了OA的基因表达谱。结果:采用瘦素诱导OA大鼠模型,观察OA软骨组织病理学特征。采用全基因组微阵列杂交技术比较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,下调660个),其中一些已知与瘦素诱导的OA表型相关。这些基因包括与MMPs相关的基因、炎症因子、生长因子、凋亡基因和成骨基因。此外,在瘦素诱导的OA软骨中检测到一些新的候选基因(如BCL2L11)的表达上调,这些基因迄今为止尚未与OA相关,这表明这些基因可能在OA分子机制中起重要作用。结论:我们的研究结果表明,瘦素诱导的OA的发病机制涉及多个基因的表达调节,尽管其潜在的分子机制有待进一步研究。需要进一步研究瘦素诱导的基因表达变化,从而对OA发病的分子机制有新的认识。
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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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