Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2017
Deferoxamine-Induced Migration and Odontoblast Differentiation via ROS-Dependent Autophagy in Dental Pulp Stem Cells.
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СтатьяОтозванная публикацияНазвание и аннотация: Перевод в очереди
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Wang Xuan, Wu Tian Tian, Jiang Long, Rong Du, Zhu Ya Qin
Аннотация
BACKGROUND/AIMS: As a vital degradation and recycling system, autophagy plays an essential role in regulating the differentiation of stem cells. We previously showed that iron chelator deferoxamine (DFO) could promote the repair ability of dental pulp stem cells (DPSCs). Here, we investigated the effect of DFO in autophagy and the role of autophagy in regulating the migration and odontoblast differentiation of DPSCs.
METHODS: Transmission electron microscopy, immunofluorescence staining and western blotting were performed to evaluate the autophagic activity of DPSCs. Transmigration assay, alkaline phosphatase staining/activity, alizarin red S staining and quantitative PCR were performed to examine the migration and odontoblast differentiation of DPSCs. Reactive oxygen species (ROS) levels and the effects of ROS scavenger in autophagy induction were also detected. Autophagy inhibitors (3-MA and bafilomycin A1) and lentiviral vectors carrying ATG5 shRNA sequences were used for autophagy inhibition.
RESULTS: Early exposure to DFO promoted the mineralization of DPSCs and increased autophagic activity. Autophagy inhibition suppressed DFO-induced DPSC migration and odontoblast differentiation. Furthermore, DFO treatment could induce autophagy partly through hypoxia-inducible factor 1α/B cell lymphoma 2/adenovirus E1B 19K-interacting protein 3 (HIF-1α/BNIP3) pathway in a ROS-dependent manner.
CONCLUSION: DFO increased DPSC migration and differentiation, which might be modulated through ROS-induced autophagy.
METHODS: Transmission electron microscopy, immunofluorescence staining and western blotting were performed to evaluate the autophagic activity of DPSCs. Transmigration assay, alkaline phosphatase staining/activity, alizarin red S staining and quantitative PCR were performed to examine the migration and odontoblast differentiation of DPSCs. Reactive oxygen species (ROS) levels and the effects of ROS scavenger in autophagy induction were also detected. Autophagy inhibitors (3-MA and bafilomycin A1) and lentiviral vectors carrying ATG5 shRNA sequences were used for autophagy inhibition.
RESULTS: Early exposure to DFO promoted the mineralization of DPSCs and increased autophagic activity. Autophagy inhibition suppressed DFO-induced DPSC migration and odontoblast differentiation. Furthermore, DFO treatment could induce autophagy partly through hypoxia-inducible factor 1α/B cell lymphoma 2/adenovirus E1B 19K-interacting protein 3 (HIF-1α/BNIP3) pathway in a ROS-dependent manner.
CONCLUSION: DFO increased DPSC migration and differentiation, which might be modulated through ROS-induced autophagy.
Предметные рубрики MeSH
AdenineAdolescentAutophagyAutophagy-Related Protein 5Beclin-1Cell DifferentiationCell MovementCell ProliferationCells, CulturedDeferoxamineDental PulpHumansHypoxia-Inducible Factor 1, alpha SubunitMacrolidesMembrane ProteinsMicroscopy, Electron, TransmissionMicrotubule-Associated ProteinsOdontoblastsProto-Oncogene ProteinsRNA InterferenceRNA, Small InterferingReactive Oxygen SpeciesStem CellsYoung Adult