Li Xinzhu, Xu Wenan, Lin Xiaoyu, Wu Jingyi, Wu Buling
Department of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Department of Pediatric Dentistry, Shenzhen Stomatology Hospital (Pingshan), Southern Medical University, Shenzhen, China.
Front Cell Dev Biol. 2022 Aug 11;10:921364. doi: 10.3389/fcell.2022.921364. eCollection 2022.
Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) belongs to the long non-coding RNA (LncRNA) family. LncRNA-MALAT1 is expressed in a variety of tissues and is involved in a variety of diseases and biological processes. Although LncRNA-MALAT1 is upregulated in a high-glucose microenvironment and may participate in odontogenic differentiation, the underlying mechanism is not yet well elucidated. Here, we show that MALAT1 was mainly expressed in the cytoplasm of dental pulp cells (DPCs) hybridization. In addition, high levels of mineralization-related factors, namely, tumor growth factors 1 and 2 (TGFβ-1 and TGFβ-2), bone morphogenetic proteins 2 and 4 (BMP2 and BMP4), bone morphogenetic protein receptor 1 (BMPR1), SMAD family member 2 (SMAD2), runt-related transcription factor 2 (RUNX2), Msh homeobox 2 (MSX2), transcription factor SP7 (SP7), alkaline phosphatase (ALP), dentin matrix acidic phosphoprotein 1 (DMP1), and dentin sialophosphoprotein (DSPP), were expressed, and MALAT1 was significantly overexpressed in DPCs 7 and 14 days after mineralization induction in a high-glucose microenvironment, but only TGFβ-1, BMP2, MSX2, SP7, ALP, and DSPP were significantly downregulated in DPCs after MALAT1 inhibition. MALAT1 may participate in the mineralization process of DPCs by regulating multiple factors (TGFβ-1, BMP2, MSX2, SP7, ALP, and DSPP).
转移相关的肺腺癌转录本1（MALAT1）属于长链非编码RNA（LncRNA）家族。LncRNA-MALAT1在多种组织中表达，并参与多种疾病和生物学过程。尽管LncRNA-MALAT1在高糖微环境中上调且可能参与牙源性分化，但其潜在机制尚未完全阐明。在此，我们通过杂交显示MALAT1主要在牙髓细胞（DPCs）的细胞质中表达。此外，高水平的矿化相关因子，即肿瘤生长因子1和2（TGFβ-1和TGFβ-2）、骨形态发生蛋白2和4（BMP2和BMP4）、骨形态发生蛋白受体1（BMPR1）、SMAD家族成员2（SMAD2）、 runt相关转录因子2（RUNX2）、Msh同源盒2（MSX2）、转录因子SP7（SP7）、碱性磷酸酶（ALP）、牙本质基质酸性磷酸蛋白1（DMP1）和牙本质涎磷蛋白（DSPP）表达，并且在高糖微环境中矿化诱导后7天和14天，MALAT1在DPCs中显著过表达，但在MALAT1抑制后，只有TGFβ-1、BMP2、MSX2、SP7、ALP和DSPP在DPCs中显著下调。MALAT1可能通过调节多种因子（TGFβ-1、BMP2、MSX2、SP7、ALP和DSPP）参与DPCs的矿化过程。
