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
  • Gene Knockdown Techniques*
  • Hepcidins/chemistry
  • Hepcidins/genetics*
  • Hepcidins/metabolism
  • Iron/metabolism
  • Iron Overload/complications
  • Iron Overload/genetics*
  • Iron Overload/metabolism
  • Iron Overload/pathology
  • Morpholinos/genetics
  • Osteoblasts/metabolism
  • Osteoblasts/pathology
  • Osteogenesis*
  • Phylogeny
  • RNA, Messenger/genetics
  • Zebrafish/genetics
  • Zebrafish/physiology*
  • Zebrafish Proteins/chemistry
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed: 27233600 Full text @ Biochem. Biophys. Res. Commun.
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.