Hepcidin1 Knockout Mice Display Defects in Bone Microarchitecture and Changes of Bone Formation Markers

被引：55

作者：

Shen, Guang Si ^{[1
]}

Yang, Qing ^{[2
]}

Jian, Jing Long ^{[2
]}

Zhao, Guo Yang ^{[1
]}

Liu, Lu Lin ^{[1
]}

Wang, Xiao ^{[1
]}

Zhang, Wen ^{[3
]}

Huang, Xi ^{[2
]}

Xu, You Jia ^{[1
]}

机构：

[1] Soochow Univ, Dept Orthopaed, Affiliated Hosp 2, Suzhou 215004, Peoples R China

[2] NYU, Sch Med, Div Rheumatol, Dept Med,NYU Hosp Joint Dis, New York, NY 10016 USA

[3] Soochow Univ, Inst Orthopaed, Suzhou 215000, Peoples R China

来源：

CALCIFIED TISSUE INTERNATIONAL | 2014年 / 94卷 / 06期

基金：

中国国家自然科学基金;

关键词：

Bone microarchitecture; Bone turnover; Hepcidin; Iron; Osteoporosis; IRON OVERLOAD; OXIDATIVE STRESS; TRANSFERRIN RECEPTOR-2; POSTMENOPAUSAL WOMEN; MINERAL DENSITOMETRY; HOMOCYSTEINE LEVELS; HEMOCHROMATOSIS; OSTEOPOROSIS; METABOLISM; DIFFERENTIATION;

D O I：

10.1007/s00223-014-9845-8

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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.

引用

页码：632 / 639

页数：8

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