Department of Prosthetics, The Affiliated Stomatology Hospital of Zunyi Medical University, Zunyi Medical University, Zunyi, China.
Key Laboratory of Oral Disease Research in General Colleges and Universities of Guizhou Province, Zunyi Medical University, Zunyi, China.
J Oral Pathol Med. 2021 Feb;50(2):236-243. doi: 10.1111/jop.13131. Epub 2020 Dec 31.
Temporomandibular joint osteoarthritis (TMJOA) is a degenerative disease that gradually affects the articular cartilage, synovium, and bone structure. To date, the molecular mechanism of TMJOA pathogenesis remains unclear. The aim of this study was to explore the biological function of the micro-ribonucleic acid 101a-3p (miR-101a-3p) and its role in TMJOA.
We detected the effect of interleukin-1β (IL-1β) on chondrocyte proliferation using Cell Counting Kit-8 (CCK-8) technology. Using quantitative polymerase chain reaction (qPCR), we detected transcription levels of miR-101a-3p in a rat model with TMJOA and inflamed chondrocytes, as well as in a group of normal rats. The effect of miR-101a-3p on apoptosis was examined in vitro using flow cytometry (FCM). We then analyzed the target of miR-101a-3p via bioinformatics and confirmed it using a luciferase reporter assay (LRA).
We showed that IL-1β could inhibit proliferation of chondrocytes. We found that miR-101a-3p levels were significantly lower in the rat inflammation model with TMJOA and inflamed chondrocytes than in the normal group. Additionally, miR-101a-3p substantially promoted apoptosis of chondrocytes, and both bioinformatic analyses and LRA found that this miRNA targeted the genes ubiquitin-conjugating enzyme 2D1 (UBE2D1) and Frizzled class receptor 4 (FZD4).
Our results suggested that miR-101a-3p was involved in the pathogenesis of TMJOA and that its mechanism was probably interaction with its target genes UBE2D1 and FZD4.
颞下颌关节骨关节炎（TMJOA）是一种退行性疾病，逐渐影响关节软骨、滑膜和骨结构。迄今为止，TMJOA 发病机制的分子机制仍不清楚。本研究旨在探讨微小核糖核酸 101a-3p（miR-101a-3p）的生物学功能及其在 TMJOA 中的作用。
我们使用细胞计数试剂盒-8（CCK-8）技术检测白细胞介素-1β（IL-1β）对软骨细胞增殖的影响。通过定量聚合酶链反应（qPCR）检测 TMJOA 大鼠模型和炎症软骨细胞以及正常大鼠中 miR-101a-3p 的转录水平。通过流式细胞术（FCM）体外检测 miR-101a-3p 对细胞凋亡的影响。然后通过生物信息学分析 miR-101a-3p 的靶标，并通过荧光素酶报告基因分析（LRA）进行验证。
我们表明 IL-1β 可以抑制软骨细胞的增殖。我们发现 TMJOA 大鼠炎症模型和炎症软骨细胞中的 miR-101a-3p 水平明显低于正常组。此外，miR-101a-3p 显著促进软骨细胞凋亡，生物信息学分析和 LRA 均发现该 miRNA 靶向泛素结合酶 2D1（UBE2D1）和卷曲受体 4（FZD4）基因。
我们的结果表明，miR-101a-3p 参与 TMJOA 的发病机制，其机制可能与其靶基因 UBE2D1 和 FZD4 相互作用有关。
