新兴研究阐明了非编码RNA（lncRNA）在各种病理进展中的关键作用。本研究旨在研究lncRNA转移相关肺腺癌转录本1（MALAT1）和miRNA-124在成骨细胞分化中的作用，为牙周炎的病理发病提供新的线索或证据。我们构建了一个成骨细胞-成骨破骨细胞跨膜共培养系统和成骨细胞来源的外泌体（OB-exo）干预模型。我们评估了成骨破骨细胞生成以及lncRNA-MALAT1和miRNA-124的水平。通过细胞转染、定量实时反转录PCR（RT-qPCR）、Western印迹和双荧光素酶报告基因实验，调查了lncRNA MALAT1靶向miR-124调控成骨破骨细胞分化的机制。我们分离和鉴定了成骨细胞来源的外泌体。共培养和OB-exo干预可以促进成骨破骨细胞生成，并显著上调MALAT1的表达水平，而miR-124的水平相反。细胞转染小干扰RNA（si-MALAT1）和miR-124模拟剂可降低TRAP+成骨破骨细胞的形成并抑制NFATc1的表达。然而，转染miR-124抑制剂和si-MALAT1时，效果会逆转。双荧光素酶报告基因实验证实了MALAT1和miR-124以及miR-124和NFATc1之间的结合位点。lncRNA MALAT1通过竞争miR-124结合以调控NFATc1表达，作为内源性海绵发挥作用，加速成骨破骨细胞生成的进展。©2023 Zhang等

Emerging studies have explained the crucial role of non-coding RNA (lncRNA) in various pathological progressions. The study was designed to examine the role of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and miRNA-124 in the differentiation of osteoclasts, to provide new clues or evidences for the pathogenesis of periodontitis.We constructed an osteoblast-osteoclast Transwell co-culture system and osteoblast-derived exosomes (OB-exo) intervention model. We assessed the osteoclastogenesis as well as the level of lncRNA-MALAT1 and miRNA-124. The mechanism for lncRNA MALAT1 targeting miR-124 modulating the differentiation of osteoclasts was investigated by cell transfection, quantitative real-time reverse transcription PCR (RT-qPCR), Western blot, and Dual-Luciferase reporter assays.Osteoblast-derived exosomes were isolated and identified. Co-culture and OB-exo intervention can promote osteoclastogenesis, also significantly up-regulate the expression of MALAT1, while the level of miR-124 is the opposite. Transfection of cells with small interfering RNA (si-MALAT1) and miR-124 mimic decreased the formation of TRAP+ osteoclasts and inhibited the expression of NFATc1. However, the effect was reversed when transfected with miR-124 inhibitor and si-MALAT1. The Dual-Luciferase reporter assay confirmed the binding sites between MALAT1 and miR-124, and miR-124 and NFATc1.LncRNA MALAT1 functioned as an endogenous sponge by competing for miR-124 binding to regulate NFATc1 expression, accelerating the progression of osteoclastogenesis.© 2023 Zhang et al.