PUBLICATION
Hepcidin inhibition on the effect of osteogenesis in zebrafish
- Authors
- Jiang, Y., Yan, Y., Wang, X., Zhu, G., Xu, Y.J.
- ID
- ZDB-PUB-160529-8
- Date
- 2016
- Source
- Biochemical and Biophysical Research Communications 476(1): 1-6 (Journal)
- Registered Authors
- Yan, Yi-Lin
- Keywords
- Hepcidin, Iron overload, Morpholino, Zebrafish
- MeSH Terms
-
- Zebrafish/genetics
- Zebrafish/physiology*
- Iron Overload/complications
- Iron Overload/genetics*
- Iron Overload/metabolism
- Iron Overload/pathology
- Gene Knockdown Techniques*
- Bone and Bones/metabolism
- Bone and Bones/pathology
- Morpholinos/genetics
- RNA, Messenger/genetics
- Hepcidins/chemistry
- Hepcidins/genetics*
- Hepcidins/metabolism
- Osteoblasts/metabolism
- Osteoblasts/pathology
- Amino Acid Sequence
- Iron/metabolism
- Osteogenesis*
- Down-Regulation
- Animals
- Phylogeny
- Zebrafish Proteins/chemistry
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 27233600 Full text @ Biochem. Biophys. Res. Commun.
Citation
Jiang, Y., Yan, Y., Wang, X., Zhu, G., Xu, Y.J. (2016) Hepcidin inhibition on the effect of osteogenesis in zebrafish. Biochemical and Biophysical Research Communications. 476(1):1-6.
Abstract
Iron overload, as a risk factor for osteoporosis, can result in the up-regulation of Hepcidin, and Hepcidin knockout mice display defects in their bone microarchitecture. However, the molecular and genetic mechanisms underlying Hepcidin deficiency-derived bone loss remain unclear. Here, we show that hepcidin knockdown in zebrafish using morpholinos leads to iron overload. Furthermore, a mineralization delay is observed in osteoblast cells in hepcidin morphants, and these defects could be partially restored with microinjection of hepcidin mRNA. Quantitative real-time PCR analyses revealed the osteoblast-specific genes alp, runx2a, runx2b, and sp7 in morphants are down-regulated. Furthermore, we confirmed qRT-PCR results by in situ hybridization and found down-regulated genes related to osteoblast function in hepcidin morphants. Most importantly, we revealed that hepcidin was capable of removing whole-body iron which facilitated larval recovery from the reductions in bone formation and osteogenesis induced by iron overload.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping