ZFIN ID: ZDB-PUB-160529-8 |
Hepcidin inhibition on the effect of osteogenesis in zebrafish
Jiang, Y., Yan, Y., Wang, X., Zhu, G., Xu, Y.J.
Date: | 2016 |
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Source: | Biochemical and Biophysical Research Communications 476(1): 1-6 (Journal) |
Registered Authors: | Yan, Yi-Lin |
Keywords: | Hepcidin, Iron overload, Morpholino, Zebrafish |
MeSH Terms: |
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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.
ADDITIONAL INFORMATION
- Genes / Markers (7)
- Morpholino (2)
- Expression and Phenotype Data
- Fish (2)
- Orthology (2)