Effects of Deferoxamine on the Repair Ability of Dental Pulp Cells In Vitro
| Autor: | Jun-jun Zhao, Ya Yang, Tian-tian Wu, Weiwei Peng, Li-Fen Li, Ya-Qin Zhu, Donglin Qu, Rong Du, Zhuo-Jun Zhou, Long Jiang |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Pathology
medicine.medical_specialty Adolescent Cell Survival Osteocalcin Cell Culture Techniques Siderophores Tetrazolium Salts Deferoxamine Biology Young Adult Calcification Physiologic Cell Movement Explant technique medicine Humans Regeneration Coloring Agents General Dentistry Cells Cultured Dental Pulp Cell Proliferation Fluorescent Dyes Odontoblasts Cell Differentiation Hypoxia (medical) Alkaline Phosphatase Hypoxia-Inducible Factor 1 alpha Subunit Cell Hypoxia In vitro Odontogenic Blot Thiazoles Cancer research medicine.symptom medicine.drug |
| Zdroj: | Journal of Endodontics. 40:1100-1104 |
| ISSN: | 0099-2399 |
| DOI: | 10.1016/j.joen.2013.12.016 |
| Popis: | Introduction In previous studies, we found that hypoxia promoted the mineralization of dental pulp cells (DPCs). However, the clinical application of hypoxia as a therapy is questionable or unfeasible. Deferoxamine (DFO), a medication for iron overload, has also been shown to induce hypoxia. The purpose of this study was to investigate the effects of DFO on the repair ability of DPCs. Methods DPCs were obtained by using a tissue explant technique in vitro and were treated with different concentrations of DFO or hypoxia culture for 2 days. The viability, proliferation, migration, and odontogenic differentiation of DPCs were assayed and analyzed. The expression of hypoxia-inducible factor 1-alpha (HIF-1α) was assessed through Western blotting. Results Ten micromolars of DFO enhanced the expression of HIF-1α similarly to hypoxia and did not affect the viability of DPCs for 2 days. Furthermore, the proliferation, migration, and odontogenic differentiation of DPCs were promoted by DFO. Conclusions These results suggest that DFO might improve the repair ability of DPCs by HIF-1α. |
| Databáze: | OpenAIRE |
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