目的:对比兔膝关节前交叉韧带(ACL)和内侧副韧带(MCL)部分损伤前、后内源性竞争性长链非编码核糖核酸(lncRNA)与信使核糖核酸(mRNA)的差异表达,探索阻碍ACL内源性修复可能的分子机制.方法:对兔部分损伤ACL和MCL后的RNA进行测序,获得差异表达lncRNA和差异表达mRNA,并用qRT-PCR验证,随后进行京都基因和基因组百科全书(KEGG)和基因本体论(GO)分析,构建ceRNA网络.结果:共获得853个差异表达的lncRNA和994个差异表达的mRNA.GO和KEGG分析结果显示,差异表达的lncRNA在炎症反应、细胞外基质与受体的相互作用和细胞增殖方面差异较大,差异表达的mRNA在细胞因子活化和细胞黏附具有较大差异.ACL与MCL部分损伤后的核心基因差异显著.结论:兔部分损伤ACL与MCL之间的lncRNA及mRNA的表达存在明显差异,为ACL损伤内源性修复障碍机制的分子层面研究提供了更多的理论依据.
Objective:To compare the differential expression of endogenous competitive long-chain non-coding ribonucleic acid(lncRNA)with messenger ribonucleic acid(mRNA)before and after partial injury of the anterior cruciate ligament(ACL)and medial collateral ligament(MCL)in knee joint of rabbits and to explore the possible molecular mechanisms impeding the endogenous repair of the ACL.Methods:RNA after partial injury of ACL and MCL in rabbits was sequenced to obtain differentially expressed lncRNAs and differentially expressed mRNAs and verified by qRT-PCR,followed by Kyoto Encyclopaedia of Genes and Genomes(KEGG)and Gene Ontology(GO)analyses for the construction of a ceRNA network.Results:A total of 853 differential lncRNAs and 994 differential mRNAs were obtained.GO and KEGG analyses showed that the differential lncRNAs differed significantly in inflammatory responses,extracellular matrix-receptor interactions,and cell proliferation,and the differential mRNAs differed significantly in cytokine activation and cell adhesion.Significant differences in core genes were found between the ACL and the MCL after partial injury.Conclusion:Significant differences in lncRNAs and mRNAs between partially injured ACL and MCL in rabbits provide more theoretical basis for the molecular level study of the mechanism of endogenous repair disorders in ACL injury.
于涵;李一帆;李彬;温昱
中国医科大学,基础医学院组织学与胚胎学教研室,沈阳 110122中国医科大学,附属盛京医院关节外科与运动医学科,沈阳 110122
膝关节;前交叉韧带;内侧副韧带;长链非编码RNA;生物信息学;兔
knee joint;anterior cruciate ligament;medial collateral ligament;long non-coding RNA;bioinformatics;rabbit
《解剖学杂志》 2023 (006)
476-483,544 / 9
沈阳市科学计划项目(20-205-4-078)
10.3969/j.issn.1001-1633.2023.06.003
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