Hepcidin protects against iron overload-induced inhibition of bone formation in zebrafish.

Abstract:

:Iron overload increases the risk of osteoporosis, which leads to an increase in the incidences of bone fracture after menopause. In vitro studies have demonstrated that excess iron can inhibit osteoblast activity. Hepcidin, a central regulator of iron homeostasis, prevents iron overload, and thus, it is considered to have anti-osteoporosis effects. In this study, a zebrafish model was employed to investigate the therapeutic role of hepcidin in iron overload-induced inhibition of bone formation. Our results show that ferric ammonium citrate (FAC) treatment decreased osteoblast-specific gene expression (runx2a, runx2b, and bglap) and bone mineralization in the zebrafish embryo, accompanied with increased whole-body iron levels and oxidative stress. Bone mineralization and osteoblast-specific gene expression increased with the microinjection of hepcidin-flag Capped-mRNA into zebrafish embryos. Moreover, the whole-body iron content and oxidative stress in the iron-overloaded zebrafish embryos decreased when microinjection of hepcidin preceded the FAC treatment. Therefore, our study suggests that hepcidin could prevent and rescue reduced bone formation caused by FAC treatment by preventing iron absorption.

journal_name

Fish Physiol Biochem

authors

Jiang Y,Chen B,Yan Y,Zhu GX

doi

10.1007/s10695-018-0568-z

subject

Has Abstract

pub_date

2019-02-01 00:00:00

pages

365-374

issue

1

eissn

0920-1742

issn

1573-5168

pii

10.1007/s10695-018-0568-z

journal_volume

45

pub_type

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