Vitamin D may assist the UPR against sodium fluoride-induced damage by reducing RIPK1, ATG5, BECN1, oxidative stress and increasing caspase-3 in the osteoblast MC3T3-E1 cell line

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dc.contributor.authorYüksek, Veysel
dc.contributor.authorDede, Semiha
dc.contributor.authorÇetin, Sedat
dc.contributor.authorUsta, Ayşe
dc.contributor.authorTaşpınar, Mehmet
dc.date.accessioned2023-09-27T05:31:47Z
dc.date.available2023-09-27T05:31:47Z
dc.date.issued2023
dc.departmentTıp Fakültesi
dc.description.abstractOut of all measure systemic exposure to fluorides can cause defect of skeletal and dental fluorosis. Endoplasmic reticulum (ER) stress is caused by fluorine-induced oxidative stress and importance of vitamin D in its prevention is not known enough in bone cells. This study was carried out to investigate fluorine-induced oxidative stress, ER stress, and death pathways and the effect of vitamin D on them. Methods: MC3T3-E1 mouse osteoblast cell line was used as the material of the study. The NaF and vitamin D concentrations were determined by the MTT assay. NaF treatments and vitamin D supplementation (pre-add, co-add, and post-add) was administered in the cell line at 24th and 48th hours. The expression of the genes in oxidative stress, ER stress, and death pathways was determined using RT-qPCR and Western blotting techniques. Results: Vitamin D significantly reduced mRNA expression levels of SOD2, CYGB, ATF6, PERK, IRE1, ATG5 and BECN1 whereas caused an increase in levels GPX1, SOD1, NOS2 and Caspase-3 in MC3T3-E1 mouse osteoblast cell line of NaF-induced. In addition, GPX1, SOD1, ATF6, PERK, IRE1, BECN1, Caspase-3 and RIPK1 protein levels were examined by Western blot analysis, and it was determined that vitamin D decreased IRE1 and PERK protein levels, but increased GPX1, SOD1, ATF6 and Caspase-3 protein levels. Conclusion: The findings of the study suggest that vitamin D has protective potential against NaF-induced cytotoxicity reasonably through the attenuation of oxidative stress, ER stress, ATG5, IRE1 and by increasesing caspase-3 in vitro conditions.
dc.identifier.doi10.1016/j.jtemb.2023.127293
dc.identifier.issn0946-672X
dc.identifier.pmid37677921
dc.identifier.scopusqualityQ1
dc.identifier.urihttps:/dx.doi.org10.1016/j.jtemb.2023.127293
dc.identifier.urihttps://hdl.handle.net/20.500.12451/10968
dc.identifier.volume80en_US
dc.identifier.wosWOS:001091364200001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherElsevier GmbH
dc.relation.ispartofJournal of Trace Elements in Medicine and Biology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectFluoride Cytotoxicity
dc.subjectVitamin D
dc.subjectER Stress
dc.subjectOxidative Stress
dc.subjectOsteoblast
dc.titleVitamin D may assist the UPR against sodium fluoride-induced damage by reducing RIPK1, ATG5, BECN1, oxidative stress and increasing caspase-3 in the osteoblast MC3T3-E1 cell line
dc.typeArticle

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