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MiRNA expression profile in HOS cells exposed to sodium fluoride

ABSTRACT: Fluorosis is caused due to excess of fluoride intake over a long period of time. Aberrant change in RUNX2-mediated signaling cascade is one of the decisive steps during the pathogenesis of fluorosis. Till date, role of fluoride on the epigenetic alterations is not studied. In the present study, global expression profiling ofshort non-coding RNAs, in particular miRNAs and snoRNAs was carried out in NaF treated HOS cells to understand their possible role in the development of fluorosis. RT-PCR and insilico hybridization revealed that miR-124 and miR-155 can be directly involved in the transcriptional regulation of RUNX2 and RANKL genes. Compare to control, C/D box analysis revealed mark 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 also state that the alterations in UG dinucleotides and D-box sequences of snoRNAs could be due to NaF exposure.

ORGANISM(S): synthetic construct Homo sapiens

PROVIDER: GSE57550 | GEO | 2015/01/01

SECONDARY ACCESSION(S): PRJNA246687

REPOSITORIES: GEO

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miRNA expression profile in HOS cells exposed to sodium fluoride

Project description:Fluorosis is caused due to excess of fluoride intake over a long period of time. Aberrant change in RUNX2-mediated signaling cascade is one of the decisive steps during the pathogenesis of fluorosis. Till date, role of fluoride on the epigenetic alterations is not studied. In the present study, global expression profiling ofshort non-coding RNAs, in particular miRNAs and snoRNAs was carried out in NaF treated HOS cells to understand their possible role in the development of fluorosis. RT-PCR and insilico hybridization revealed that miR-124 and miR-155 can be directly involved in the transcriptional regulation of RUNX2 and RANKL genes. Compare to control, C/D box analysis revealed mark 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 also state that the alterations in UG dinucleotides and D-box sequences of snoRNAs could be due to NaF exposure. HOS cells grown on MEM media were treated with sodium fluoride and total RNA was isolated from cells after one month of chronic exposure; Cells grown on six 25mm flask. two replicates of control and two different concentration of exposed samples; two replicate are served as control

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