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Long Noncoding RNA Expression Profiles of Periodontal Ligament Stem Cells from the Periodontitis Microenvironment in Response to Static Mechanical Strain

机译:牙周炎微观环境的长期非编码RNA表达谱响应静态机械菌株

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During the period of orthodontic tooth movement, periodontal ligament stem cells (PDLSCs) play an important role in transducing mechanical stimulation and tissue remodeling. However, our previous studies verified that the periodontitis microenvironment causes damage to the biological functions of PDLSCs and abnormal mechanical sensitivity. Long noncoding RNAs (lncRNAs) participate in the inflammatory pathogenesis and development of many diseases. Whether lncRNAs are abnormally expressed in PDLSCs obtained from periodontal tissues of periodontitis patients (PPDLSCs) and whether putative lncRNAs participate in the mechanotransductive process in PDLSCs remain poorly understood. First, we subjected PDLSCs obtained from healthy periodontal tissues (HPDLSCs) and PPDLSCs to static mechanical strain (SMS) with 12% elongation at 0.1?Hz frequency using an FX-4000T system and screened overall lncRNA profiles in both cell types by microarray. Among lncRNAs with a fold , 27 lncRNAs were upregulated in strained HPDLSCs, and 16 lncRNAs (9 upregulated and 7 downregulated) were detected in strained PPDLSCs. For mRNAs with , we detected 25 upregulated mRNAs and one downregulated mRNA in strained HPDLSCs and 7 upregulated and 5 downregulated mRNAs in strained PPDLSCs. Further enrichment analysis showed that, unlike HPDLSCs with annotations principally involving transduction-associated signaling pathways, dysregulated mRNAs in PPDLSCs are mainly responsible for pathological conditions. Moreover, coexpressed lncRNA-mRNA networks confirmed the pathological state and exacerbated inflammatory conditions in strained PPDLSCs. Taken together, when compared with strained HPDLSCs, various lncRNAs and mRNAs were dysregulated in PPDLSCs under mechanical forces, implicating the response of lncRNAs in PPDLSCs to mechanical stress. Moreover, we provide potential lncRNA targets, which may contribute to future intervention strategies for orthodontic treatment in periodontitis patients.
机译:在正畸牙齿运动期间,牙周韧带干细胞(PDLSCs)在转换机械刺激和组织重塑方面发挥着重要作用。然而,我们以前的研究证实牙周炎微环境导致PDLSCs的生物功能和机械敏感性异常损伤。长时间的NOODING RNA(LNCRNA)参与炎症发病机制和许多疾病的发育。 LNCRNA是否在从牙周炎患者(PPDLSCs)的牙周组织中获得的PDLSC中异常表达,并且推定的LNCRNA参与PDLSC中的机械调节过程仍然很清楚。首先,我们使用FX-4000T系统将从健康牙周组织(HPDLSC)和PPDLSC和PPDLSC的PPDLSC和PPDLSC以0.1Ω·赫兹频率的伸长率为12%的伸长率,并通过微阵列筛选在两种细胞类型中的整体LNCRNA曲线。在具有折叠的LNCRNA中,在应变的HPDLSC中升高27个LNCRNA,并在应变PPDLSC中检测到16个LNCRNA(90次上调和7下调)。对于MRNA,我们检测到25个上调的MRNA和紧张的HPDLSCs中的一个下调mRNA和7个上调和5个紧张的PPDLSC中的下调MRNA。进一步的富集分析表明,与主要涉及转导相关的信号通路的注释不同的HPDLSC,PPDLSC中的失调MRNA主要负责病理条件。此外,共表达的LNCRNA-mRNA网络确认了应变PPDLSC中的病理状态和加剧炎症病症。与紧张的HPDLSC相比,在与应变的HPDLSC相比,在机械力下的PPDLSC中发现各种LNCRNA和MRNA,暗示LNCRNA在PPDLSCS中的响应机械应力。此外,我们提供潜在的LNCRNA靶标,这可能有助于在牙周炎患者中进行正畸治疗的未来干预策略。

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