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Deferoxamine-Induced Migration and Odontoblast Differentiation via ROS-Dependent Autophagy in Dental Pulp Stem Cells.
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- Author(s): Wang X; Wu TT; Jiang L; Rong D; Zhu YQ
- Source:
Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology [Cell Physiol Biochem] 2017; Vol. 43 (6), pp. 2535-2547. Date of Electronic Publication: 2017 Nov 01.
- Publication Type:
Journal Article; Retracted Publication
- Language:
English
- Additional Information
- Source:
Publisher: Cell Physiol Biochem Press GmbH & Co KG Country of Publication: Germany NLM ID: 9113221 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1421-9778 (Electronic) Linking ISSN: 10158987 NLM ISO Abbreviation: Cell Physiol Biochem Subsets: MEDLINE
- Publication Information:
Publication: 2019- : Düsseldorf, Germany : Cell Physiol Biochem Press GmbH & Co KG
Original Publication: Basel ; New York : S. Karger, 1991-2018.
- Subject Terms:
- Abstract:
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.
(© 2017 The Author(s). Published by S. Karger AG, Basel.)
- Comments:
Retraction in: Cell Physiol Biochem. 2023 Aug 31;57(4):313. (PMID: 37697993)
- Contributed Indexing:
Keywords: Cell biology; Cell differentiation; Endodontics; Odontogenesis; Pulp biology; Regeneration
- Accession Number:
0 (Autophagy-Related Protein 5)
0 (BNIP3 protein, human)
0 (Beclin-1)
0 (Hypoxia-Inducible Factor 1, alpha Subunit)
0 (MAP1LC3A protein, human)
0 (Macrolides)
0 (Membrane Proteins)
0 (Microtubule-Associated Proteins)
0 (Proto-Oncogene Proteins)
0 (RNA, Small Interfering)
0 (Reactive Oxygen Species)
116764-51-3 (bafilomycin A)
5142-23-4 (3-methyladenine)
J06Y7MXW4D (Deferoxamine)
JAC85A2161 (Adenine)
- Publication Date:
Date Created: 20171114 Date Completed: 20180118 Latest Revision: 20230912
- Publication Date:
20231215
- Accession Number:
10.1159/000484506
- Accession Number:
29131087
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