Department of Stomatology, First Hospital Affiliated to Hebei North University, Zhangjiakou, Hebei, China.
Department of Stomatology, Medical College, Zhangjiakou University, Zhangjiakou, China.
Biotechnol Genet Eng Rev. 2024 Nov;40(3):2560-2576. doi: 10.1080/02648725.2023.2200331. Epub 2023 Apr 14.
The long non-coding RNA (LncRNA) X-inactive specific transcript (XIST) regulates the biological process of osteoclasts and the process of related diseases. This study was attempted to investigate the mechanism of LncRNA XIST acting in osteoclast formation and orthodontic induced inflammatory root resorption (OIIRR). The compression force (CF) -induced cell model and the orthodontic tooth movement (OTM) rat model were designed and established in this study. The expression of LncRNA XIST, miR-130b-3p, phosphatase and tensin homolog deleted on chromosome 10 (PTEN) as well as osteoclast related marker genes and inflammatory factors level were measured in this study. The interaction among LncRNA XIST, microRNA-130b-3p (miR-130b-3p) and PTEN were researched through luciferase activity and western blot assay. Pathological sections were used to analyze root resorption and osteoclast formation. The OTM rat model was successfully constructed, which was characterized by increased tooth spacing and increased root resorption pits. PTEN and LncRNA XIST was overexpressed in OTM group. Mechanism analysis showed that the overexpression of LncRNA XIST enhanced the PTEN level by sponging miR-130b-3p. The overexpression of LncRNA XIST increased the secretion of inflammatory factors and positive osteoclasts number, but inhibited the differentiation of osteoclasts by sponging miR-130b-3p and promoting the level of PTEN. This finding demonstrates that LncRNA XIST regulates osteoclast formation and aggravated OIIRR through miR-130b-3p/PTEN axis, suggesting that LncRNA XIST may be used as potential targets for OIIRR therapy.
长链非编码 RNA（LncRNA）X 失活特异性转录物（XIST）调节破骨细胞的生物学过程和相关疾病的发生过程。本研究旨在探讨 LncRNA XIST 在破骨细胞形成和正畸诱导炎症性牙根吸收（OIIRR）中的作用机制。本研究设计并建立了压缩力（CF）诱导的细胞模型和正畸牙齿移动（OTM）大鼠模型。本研究测量了 LncRNA XIST、miR-130b-3p、磷酸酶和张力蛋白同源物缺失的 10 号染色体（PTEN）以及破骨细胞相关标记基因和炎症因子水平的表达。通过荧光素酶活性和 Western blot 分析研究了 LncRNA XIST、微小 RNA-130b-3p（miR-130b-3p）和 PTEN 之间的相互作用。通过病理切片分析了牙根吸收和破骨细胞形成。成功构建了 OTM 大鼠模型，其特征为牙间隙增大和根吸收凹坑增多。OTM 组中 PTEN 和 LncRNA XIST 表达上调。机制分析表明，LncRNA XIST 通过海绵 miR-130b-3p 增强了 PTEN 水平。LncRNA XIST 的过表达增加了炎症因子的分泌和阳性破骨细胞数量，但通过海绵 miR-130b-3p 和促进 PTEN 水平抑制了破骨细胞的分化。这一发现表明，LncRNA XIST 通过 miR-130b-3p/PTEN 轴调节破骨细胞形成并加重 OIIRR，提示 LncRNA XIST 可能成为 OIIRR 治疗的潜在靶点。
