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
Source: Biochemical and Biophysical Research Communications 476(1): 1-6 (Journal)
Registered Authors: Yan, Yi-Lin
Keywords: Hepcidin, Iron overload, Morpholino, Zebrafish
MeSH Terms: Amino Acid Sequence; Animals; Bone and Bones/metabolism; Bone and Bones/pathology; Down-Regulation (all 25) expand
PubMed: 27233600 Full text @ Biochem. Biophys. Res. Commun.
FIGURES   (current status)
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.