Zhang Gang, Wu Yadi, Xu Dong, Yan Xinfeng
1 Department of Articular Surgery, Qianfoshan Hospital of Shandong University , Jinan, China .
2 Affiliated Hospital of Taishan Medical University , Taian, China .
DNA Cell Biol. 2016 Nov;35(11):691-695. doi: 10.1089/dna.2016.3397. Epub 2016 Aug 16.
Osteoarthritis (OA) is one of the most common prevalent chronic joint diseases. Emerging pieces of evidence have demonstrated that chondrocytes survival was closely associated with the destruction of joints in OA patients. Long noncoding RNAs (lncRNAs), defined as >200 nucleotides in length, also have been implicated in a variety of disease states. However, there are few studies on the role of lncRNAs in OA, and the pathological contributions of lncRNAs to OA remain largely unknown. In this study, we examined the expression of lncRNA UFC1 in cartilage samples from OA patients and healthy subjects, and then investigated biological function of UFC1 in OA chondrocyte. We found that the UFC1 was significantly reduced in OA patients. Functional assays demonstrated that UFC1 promotes chondrocytes proliferation and inhibits cell apoptosis. Furthermore, we found that UFC1 regulates survival of OA chondrocytes through physically association with miR-34a. Taken together, our data highlight the important roles of lncRNA UFC1 in the survival of OA chondrocytes. UFC1 may be a potential therapy for OA.
骨关节炎(OA)是最常见的慢性关节疾病之一。新出现的证据表明,软骨细胞存活与OA患者关节破坏密切相关。长度大于200个核苷酸的长链非编码RNA(lncRNAs)也与多种疾病状态有关。然而,关于lncRNAs在OA中的作用的研究很少,lncRNAs对OA的病理贡献在很大程度上仍然未知。在本研究中,我们检测了OA患者和健康受试者软骨样本中lncRNA UFC1的表达,然后研究了UFC1在OA软骨细胞中的生物学功能。我们发现OA患者中UFC1显著降低。功能分析表明,UFC1促进软骨细胞增殖并抑制细胞凋亡。此外,我们发现UFC1通过与miR-34a物理结合来调节OA软骨细胞的存活。综上所述,我们的数据突出了lncRNA UFC1在OA软骨细胞存活中的重要作用。UFC1可能是OA的一种潜在治疗方法。