Fluoride-Induced Oxidative and Inflammatory Stress in Osteosarcoma Cells: Does It Affect Bone Development Pathway?
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Oxidative stress is reported to negatively affect osteoblast cells. Present study reports oxidative and inflammatory signatures in fluoride-exposed human osteosarcoma (HOS) cells, and their possible association with the genes involved in osteoblastic differentiation and bone development pathways. HOS cells were challenged with sublethal concentration (8 mg/L) of sodium fluoride for 30 days and analyzed for transcriptomic expression. In total, 2632 transcripts associated with several biological processes were found to be differentially expressed. Specifically, genes involved in oxidative stress, inflammation, osteoblastic differentiation, and bone development pathways were found to be significantly altered. Variation in expression of key genes involved in the abovementioned pathways was validated through qPCR. Expression of serum amyloid A1 protein, a key regulator of stress and inflammatory pathways, was validated through western blot analysis. This study provides evidence that chronic oxidative and inflammatory stress may be associated with the fluoride-induced impediment in osteoblast differentiation and bone development.
KeywordsSodium fluoride Osteosarcoma cells (HOS) Oxidative stress Inflammatory stress Gene microarray Bone development
The authors are grateful to Council of Scientific and Industrial Research (CSIR), India, for providing research grant and necessary facilities under INDEPTH networking project (BSC0111). Deepa Gandhi is thankful to the Department of Science and Technology (DST), India, for the award of senior research fellowship (number IF110408). This manuscript represents CSIR-NEERI communication number KRC\2016\MAY\EHD\1.
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Conflict of Interest
The authors declare that they have no conflict of interest.
- 3.Joshi V, Joshi NK (2014) Fluorosis and its impact on public health in Jodhpur Rajasthan. Int J Basic Appl Med Sci 4:87–92Google Scholar
- 4.O’Brien CA (2010) Control of RANKL gene expression. Bone 46:911-919Google Scholar
- 8.Daiwile AP, Sivanesan S, Izzotti A, Bafana A, Naoghare PK, Arrigo P, Purohit HJ, Parmar D, Kannan K (2015) Noncoding RNAs: possible players in the development of fluorosis. BioMed Res IntGoogle Scholar
- 16.Yang RZ, Lee MJ, Hu H, Pollin TI, Ryan AS, Nicklas BJ, Snitker S, Horenstein RBB, Hull K, Goldberg NH, Goldberg AP, Shuldiner AR, Fried SK, Gong DW (2006) Acute-phase serum amyloid A: an inflammatory adipokine and potential link between obesity and its metabolic complications. PLoS Med 3:e287CrossRefPubMedPubMedCentralGoogle Scholar
- 21.Duchateau PN, Movsesyan I, Yamashita S, Sakai N, Hirano KI, Schoenhaus SA, O’Connor-Kearns PM, Spencer SJ, Jaffe RB, Redberg RF, Ishida BY, Matsuzawa Y, Kane JP, Malloy MJ (2000) Plasma apolipoprotein L concentrations correlate with plasma triglycerides and cholesterol levels in normolipidemic, hyperlipidemic, and diabetic subjects. J Lipid Res 41:1231–1236PubMedGoogle Scholar
- 35.Friedl G, Schmidt H, Rehak I, Kostner G, Schauenstein K, Windhager R (2007) Undifferentiated human mesenchymal stem cells (hMSCs) are highly sensitive to mechanical strain: transcriptionally controlled early osteo-chondrogenic response in vitro. Osteoarthr Cartil 15:1293–1300CrossRefPubMedGoogle Scholar