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Hepcidin inhibition on the effect of osteogenesis in zebrafish.

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.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Jiang Y,Yan Y,Wang X,Zhu G,Xu YJ

doi

10.1016/j.bbrc.2016.05.118

subject

Has Abstract

pub_date

2016-07-15 00:00:00

pages

1-6

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(16)30826-9

journal_volume

476

pub_type

杂志文章

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