PUBLICATION
Hepcidin protects against iron overload-induced inhibition of bone formation in zebrafish
- Authors
- Jiang, Y., Chen, B., Yan, Y., Zhu, G.X.
- ID
- ZDB-PUB-181027-6
- Date
- 2018
- Source
- Fish physiology and biochemistry 45(1): 365-374 (Journal)
- Registered Authors
- Keywords
- Bone formation, Hepcidin, Iron overload, Osteoblast, Oxidative stress, Zebrafish
- MeSH Terms
-
- Animals
- Anti-Infective Agents/pharmacology
- Bone Development/drug effects*
- Dose-Response Relationship, Drug
- Down-Regulation
- Ferric Compounds/administration & dosage
- Ferric Compounds/adverse effects*
- Ferric Compounds/pharmacology
- Gene Expression Regulation/drug effects
- Hepcidins/pharmacology*
- Iron Overload/chemically induced*
- Iron Overload/prevention & control*
- Osteoblasts/drug effects
- Osteoblasts/metabolism
- Quaternary Ammonium Compounds/administration & dosage
- Quaternary Ammonium Compounds/adverse effects*
- Quaternary Ammonium Compounds/pharmacology
- Zebrafish
- PubMed
- 30361820 Full text @ Fish Physiol. Biochem.
Citation
Jiang, Y., Chen, B., Yan, Y., Zhu, G.X. (2018) Hepcidin protects against iron overload-induced inhibition of bone formation in zebrafish. Fish physiology and biochemistry. 45(1):365-374.
Abstract
Iron overload increases the risk of osteoporosis, which leads to an increase in the incidences of bone fracture after menopause. In vitro studies have demonstrated that excess iron can inhibit osteoblast activity. Hepcidin, a central regulator of iron homeostasis, prevents iron overload, and thus, it is considered to have anti-osteoporosis effects. In this study, a zebrafish model was employed to investigate the therapeutic role of hepcidin in iron overload-induced inhibition of bone formation. Our results show that ferric ammonium citrate (FAC) treatment decreased osteoblast-specific gene expression (runx2a, runx2b, and bglap) and bone mineralization in the zebrafish embryo, accompanied with increased whole-body iron levels and oxidative stress. Bone mineralization and osteoblast-specific gene expression increased with the microinjection of hepcidin-flag Capped-mRNA into zebrafish embryos. Moreover, the whole-body iron content and oxidative stress in the iron-overloaded zebrafish embryos decreased when microinjection of hepcidin preceded the FAC treatment. Therefore, our study suggests that hepcidin could prevent and rescue reduced bone formation caused by FAC treatment by preventing iron absorption.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping