AI Article Synopsis
- Fluorosis results from prolonged excessive fluoride intake, impacting the RUNX2 signaling pathway crucial for bone development.
- Research focused on the effects of sodium fluoride (NaF) on human osteosarcoma cells, aiming to uncover its influence on noncoding RNAs like miRNAs and snoRNAs.
- The study identified miR-124 and miR-155 as potential regulators of RUNX2 and RANKL genes, with specific changes in UG dinucleotides and D-box sequences linked to NaF exposure.
Article Abstract
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 κ-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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4538412 | PMC |
| http://dx.doi.org/10.1155/2015/274852 | DOI Listing |
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