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Noncoding RNAs: Possible Players in the Development of Fluorosis

机译:非编码RNA:可能的球员在发育氟中毒

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Fluorosis is caused by excess of fluoride intake over a long period of time. Aberrant change in the Runt-related transcription factor 2 (RUNX2) mediated signaling cascade is one of the decisive steps during the pathogenesis of fluorosis. Up to date, role of fluoride on the epigenetic alterations is not studied. In the present study, global expression profiling of short noncoding RNAs, in particular miRNAs and snoRNAs, was carried out in sodium fluoride (NaF) treated human osteosarcoma (HOS) cells to understand their possible role in the development of fluorosis. qPCR and in silico hybridization revealed that miR-124 and miR-155 can be directly involved in the transcriptional regulation of Runt-related transcription factor 2 (RUNX2) and receptor activator of nuclear factor k-B ligand (RANKL) genes. Compared to control, C/D box analysis revealed marked elevation in the number of UG dinucleotides and D-box sequences in NaF exposed HOS cells. Herein, we report miR-124 and miR-155 as the new possible players involved in the development of fluorosis. We show that the alterations in UG dinucleotides and D-box sequences of snoRNAs could be due to NaF exposure.
机译:氟中毒是在很长一段时间内过量的氟化物摄入量引起的。 runt相关转录因子2(RUNX2)介导的信号级联的异常变化是氟中毒发病过程中的决定性步骤之一。迄今为止,氟化物对表观遗传改变的作用没有。在本研究中,在氟化钠(NAF)处理的人骨肉瘤(HOS)细胞中,在氟化钠(NAF)的人骨肉瘤(HOS)细胞中进行全局表达谱,特别是MiRNA和SnaNAs,以了解其在氟中止的发育中可能作用。 QPCR和硅杂交中揭示了miR-124和miR-155可以直接参与鲁代相关转录因子2(RUNX2)和核因子K-B配体(RANKL)基因的受体激活剂的转录调节。与对照相比,C / D盒子分析显示NAF暴露的HOS细胞中的UG二核苷酸和D盒序列数的显着升高。在此,我们将MIR-124和MIR-155报告为参与氟中的开发的新可能球员。我们表明,UG二核苷酸和Snornas的D-Box序列的改变可能是由于NAF暴露。

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