Laboratory for Bone and Joint Diseases, Center for Integrative Medical Sciences, RIKEN, Tokyo 108-8639, Japan.
Laboratory for Statistical and Translational Genetics, Center for Integrative Medical Sciences, RIKEN, Yokohama 230-0045, Japan; Laboratory of Complex Trait Genomics, Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo 108-8639, Japan.
Am J Hum Genet. 2023 Apr 6;110(4):638-647. doi: 10.1016/j.ajhg.2023.03.004. Epub 2023 Mar 28.
Ossification of the posterior longitudinal ligament of the spine (OPLL) is a common intractable disease that causes spinal stenosis and myelopathy. We have previously conducted genome-wide association studies for OPLL and identified 14 significant loci, but their biological implications remain mostly unclear. Here, we examined the 12p11.22 locus and identified a variant in the 5' UTR of a novel isoform of CCDC91 that was associated with OPLL. Using machine learning prediction models, we determined that higher expression of the novel CCDC91 isoform was associated with the G allele of rs35098487. The risk allele of rs35098487 showed higher affinity in the binding of nuclear proteins and transcription activity. Knockdown and overexpression of the CCDC91 isoform in mesenchymal stem cells and MG-63 cells showed paralleled expression of osteogenic genes, including RUNX2, the master transcription factor of osteogenic differentiation. The CCDC91 isoform directly interacted with MIR890, which bound to RUNX2 and decreased RUNX2 expression. Our findings suggest that the CCDC91 isoform acts as a competitive endogenous RNA by sponging MIR890 to increase RUNX2 expression.
脊柱后纵韧带骨化症(OPLL)是一种常见的难治性疾病,可导致椎管狭窄和脊髓病。我们之前对 OPLL 进行了全基因组关联研究,确定了 14 个显著的位点,但它们的生物学意义仍大多不清楚。在这里,我们研究了 12p11.22 位点,并在一个新的 CCDC91 异构体的 5'UTR 中发现了一个与 OPLL 相关的变体。使用机器学习预测模型,我们确定新型 CCDC91 异构体的高表达与 rs35098487 的 G 等位基因相关。rs35098487 的风险等位基因在核蛋白结合和转录活性方面显示出更高的亲和力。在间充质干细胞和 MG-63 细胞中敲低和过表达 CCDC91 异构体显示出成骨基因的平行表达,包括 RUNX2,成骨分化的主转录因子。CCDC91 异构体与 MIR890 直接相互作用,MIR890 结合 RUNX2 并降低 RUNX2 的表达。我们的研究结果表明,CCDC91 异构体作为竞争性内源性 RNA,通过海绵吸附 MIR890 来增加 RUNX2 的表达。