Erschienen in:
01.06.2014 | Original Research
Hepcidin1 Knockout Mice Display Defects in Bone Microarchitecture and Changes of Bone Formation Markers
verfasst von:
Guang Si Shen, Qing Yang, Jing Long Jian, Guo Yang Zhao, Lu Lin Liu, Xiao Wang, Wen Zhang, Xi Huang, You Jia Xu
Erschienen in:
Calcified Tissue International
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Ausgabe 6/2014
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Abstract
Iron accumulation is a risk factor of osteoporosis; mechanisms leading to iron-related bone loss are not fully determined. We sought to better understand the effect of chronic iron accumulation on bone over the life span in a mouse model. Hepcidin1 knockout (Hepc1
−/−) male mice and their littermate control wild type (WT) mice at 7 months old were used in this study. Serum iron and ferritin as well as iron contents in liver and femur were significantly increased in Hepc1
−/− mice compared to WT mice. We found that Hepc1
−/− mice had a phenotype of low bone mass and alteration of the bone microarchitecture, most likely caused by a decreased osteoblastic activity. Cell culture studies indicated that chronic iron accumulation decreased bone formation, probably by affecting bone morphogenetic protein signaling.