Hepcidin1 knockout mice display defects in bone microarchitecture and changes of bone formation markers

Calcif Tissue Int. 2014 Jun;94(6):632-9. doi: 10.1007/s00223-014-9845-8. Epub 2014 Mar 21.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biomarkers / analysis
  • Bone Density / physiology
  • Bone Remodeling / physiology
  • Bone and Bones / chemistry
  • Bone and Bones / metabolism
  • Bone and Bones / ultrastructure*
  • Enzyme-Linked Immunosorbent Assay
  • Ferritins / analysis
  • Ferritins / metabolism
  • Hepcidins / genetics
  • Hepcidins / metabolism*
  • Iron / analysis
  • Iron / metabolism*
  • Male
  • Mice
  • Mice, Knockout
  • Osteogenesis / physiology*
  • X-Ray Microtomography

Substances

  • Biomarkers
  • Hamp protein, mouse
  • Hepcidins
  • Ferritins
  • Iron