Zhang Chunping, Wang Peng, Jiang Pengfei, Lv Yongbin, Dong Changxia, Dai Xiuyu, Tan Lixia, Wang Zhenlin
Department of Stomatology, Yantai Yuhuangding Hospital, China.
Department of Stomatology, Dental Hospital of Yantai City, China.
Gene. 2016 Jul 25;586(2):248-53. doi: 10.1016/j.gene.2016.04.016. Epub 2016 Apr 7.
Temporomandibular joint osteoarthritis (TMJ OA) is a common and heterogeneous disease that causes painful and progressive joint degeneration, which restricts daily activities, including talking and chewing. Long noncoding RNAs (lncRNAs) are an important class of genes involved in various physiological and pathological functions, including osteoarthritis (OA).The present study aimed to identify the lncRNAs that are important in TMJ OA and their potential functions. Here, we found that HOTAIR was significantly upregulated in the synovial fluid of TMJ OA patients compared with that of normal controls. Increased HOTAIR was similarly observed in the synovial fluid of TMJ OA rabbits as compared to control rabbits. Furthermore, in interleukin-1β (IL-1β)-induced TMJ OA in vitro model (primary rabbit condylar chondrocytes), the expressions of matrix metalloproteinase (MMP)-1, MMP3, MMP9 and HOTAIR were all dramatically increased. Most importantly, knockdown of HOTAIR in IL-1β-induced TMJ OA in vitro model could not only reverse the IL-1β-stimulated expressions of MMP1, MMP3 and MMP9, but also significantly decrease the apoptosis rate induced by IL-1β in primary rabbit condylar chondrocytes. Our data provides new insight into the mechanisms of chondrocytes destruction in TMJ OA.
颞下颌关节骨关节炎（TMJ OA）是一种常见的异质性疾病，可导致疼痛性和进行性关节退变，限制包括说话和咀嚼在内的日常活动。长链非编码RNA（lncRNAs）是一类重要的基因，参与包括骨关节炎（OA）在内的各种生理和病理功能。本研究旨在鉴定在TMJ OA中起重要作用的lncRNAs及其潜在功能。在此，我们发现与正常对照组相比，TMJ OA患者滑液中HOTAIR显著上调。与对照兔相比，在TMJ OA兔的滑液中也观察到HOTAIR增加。此外，在白细胞介素-1β（IL-1β）诱导的体外模型（原代兔髁突软骨细胞）中的TMJ OA中，基质金属蛋白酶（MMP）-1、MMP3、MMP9和HOTAIR的表达均显著增加。最重要的是，在IL-1β诱导的体外模型中的TMJ OA中敲低HOTAIR不仅可以逆转IL-1β刺激的MMP1、MMP3和MMP9的表达，还可以显著降低IL-1β诱导的原代兔髁突软骨细胞的凋亡率。我们的数据为TMJ OA中软骨细胞破坏的机制提供了新的见解。
