Ectopic bone formation is the chief characteristic of ossification of the posterior longitudinal ligament (OPLL). Emerging evidence has revealed that long non-coding RNAs (lncRNAs) can regulate the osteogenic differentiation of mesenchymal stem cells (MSCs), which are the main cells responsible for bone formation. However, the role of lncRNAs in the pathogenesis of OPLL remains unclear. In this study, 725 aberrantly expressed lncRNAs and 664 mRNAs in osteogenically differentiated MSCs from OPLL patients (OPLL MSCs) were identified by microarrays and confirmed by qRT-PCR assays. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses showed that the most enriched pathways included the p53, JAK-STAT, and PI3K-Akt signaling pathways. The co-expression network showed the interactions between the aberrantly expressed lncRNAs and mRNAs in OPLL MSCs, and the potential targets and transcription factors of the lncRNAs were predicted. Our research demonstrated the aberrantly expressed lncRNA and mRNA and the potential regulatory networks involved in the ectopic bone formation of OPLL. These findings imply that lncRNAs may play a vital role in OPLL, which provides a new perspective on the pathogenesis of OPLL.

异位骨形成是后纵韧带（OPLL）骨化的主要特征。新兴证据表明，长的非编码RNA（lncRNA）可以调节间充质干细胞（MSC）的成骨分化，MSC是负责骨骼形成的主要细胞。但是，lncRNA在OPLL发病机理中的作用尚不清楚。在这项研究中，通过微阵列鉴定了来自OPLL患者的成骨分化MSC（OPLL MSC）中的725个异常表达的lncRNA和664 mRNA，并通过qRT-PCR分析进行了确认。基因本体论（GO）和《京都基因与基因组百科全书》（KEGG）途径分析显示，最丰富的途径包括p53，JAK-STAT和PI3K-Akt信号传导途径。共表达网络显示OPLL MSCs中异常表达的lncRNA和mRNA之间的相互作用，并预测了lncRNA的潜在靶标和转录因子。我们的研究证明了异常表达的lncRNA和mRNA以及潜在的调控网络参与了OPLL异位骨的形成。这些发现暗示lncRNA可能在OPLL中起重要作用，这为OPLL的发病机理提供了新的视角。