Citation:
Biochem Biophys Res Commun. 2016 May 24. pii: S0006-291X(16)30826-9. doi: 10.1016/j.bbrc.2016.05.118. [Epub ahead of print]
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.
Epub:
Yes
Link to Publication:
http://www.sciencedirect.com/science/article/pii/S0006291X16308269
Organism or Cell Type:
zebrafish
Delivery Method:
microinjection