Hepcidin inhibition on the effect of osteogenesis in zebrafish.
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.
['Jiang|Yu|Y|', 'Yan|Yilin|Y|', 'Wang|Xiao|X|', 'Zhu|Guoxing|G|', 'Xu|You-Jia|YJ|']
D000595:Amino Acid Sequence D000818:Animals D001842:Bone and Bones D015536:Down-Regulation D055785:Gene Knockdown Techniques D064451:Hepcidins D007501:Iron D019190:Iron Overload D060172:Morpholinos D010006:Osteoblasts D010012:Osteogenesis D010802:Phylogeny D012333:RNA, Messenger D015027:Zebrafish D029961:Zebrafish Proteins
Hepcidin Zebrafish Iron overload Morpholino