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BioMed Research International
Volume 2015, Article ID 274852, 10 pages
Research Article

Noncoding RNAs: Possible Players in the Development of Fluorosis

1Environmental Health Division, National Environmental Engineering Research Institute (NEERI), CSIR, Nagpur 440020, India
2Department of Health Sciences, University of Genoa, No. 5, 16126 Genoa, Italy
3IRCCS AOU San Martino IST, No. 10, 16132 Genoa, Italy
4CNR Institute for Macromolecular Studies, No. 6, 16149 Genoa, Italy
5Environmental Genomics Division, National Environmental Engineering Research Institute (NEERI), CSIR, Nagpur 440020, India
6Developmental Toxicology, Indian Institute of Toxicology Research, Lucknow 226001, India

Received 10 October 2014; Accepted 4 February 2015

Academic Editor: Luciana dos Reis Vasques

Copyright © 2015 Atul P. Daiwile et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.