促进牙周韧带干细胞（PDLSCs）成骨分化是再生牙周骨的方法之一。本研究旨在确定长链非编码RNA MALAT1是否在体外促进人类PDLSCs的成骨分化。人类PDLSCs从人牙周韧带中提取，经骨形成培养基诱导成骨分化后，转染siRNA-MALAT1、miR-93-5p模拟物和miR-93-5p抑制剂。通过RT-qPCR和西方博莱特检测骨生成相关基因的表达，通过碱性磷酸酶（ALP）活性酶活性检测酶活，通过茜素红S染色评估矿化结节的形成。以RNA免疫共沉淀（RIP）和荧光酶报告基因分析（Luciferase assays）评估MALAT1、miR-93-5p和SMAD5之间的结合。PDLSCs成骨分化后，非编码RNA肺腺癌转移相关性RNA1（MALAT1）的表达上调，而miR-93-5p的表达下调。MALAT1的敲低抑制了PDLSCs的成骨分化，MALAT1的表达与miR-93-5p的表达呈负相关。miR-93-5p通过与SMAD5特异性结合抑制了人类PDLSCs的成骨分化。MALAT1通过调节miR-93-5p / SMAD5通路调控人类PDLSC分化。© 2023 Wiley Periodicals LLC.

Promoting the osteogenic differentiation of periodontal ligament stem cells (PDLSCs) is a way to regenerate periodontal bone. This study aimed to determine whether lncRNA MALAT1 promotes the osteogenic differentiation of human PDLSCs in vitro.Human PDLSCs were extracted from the human periodontal ligament, and after osteogenic differentiation was induced using osteogenic medium, the human PDLSCs were transfected with siRNA-MALAT1, miR-93-5p mimics, and miR-93-5p inhibitors. The expression of osteogenesis-related genes was assessed by RT-qPCR and western blotting, alkaline phosphatase (ALP) activity was assessed by ALP activity assay, and the formation of mineralized nodules was assessed by alizarin red S (ARS) staining. RNA immunoprecipitation (RIP) and luciferase assays were performed to assess the binding of MALAT1, miR-93-5p, and SMAD5.The expression of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was upregulated, while that of miR-93-5p was downregulated after PDLSC osteogenic differentiation. Knockdown of MALAT1 inhibited the osteogenic differentiation of PDLSCs, and MALAT1 expression negatively correlated with miR-93-5p expression. miR-93-5p inhibited the osteogenic differentiation of human PDLSCs by specifically binding to SMAD5.MALAT1 regulates human PDLSC differentiation by regulating the miR-93-5p/SMAD5 axis.© 2023 Wiley Periodicals LLC.