Skeletal muscle hemojuvelin is dispensable for systemic iron homeostasis.

Published

Journal Article

Hepcidin, a hormone produced mainly by the liver, has been shown to inhibit both intestinal iron absorption and iron release from macrophages. Hemojuvelin, a glycophosphatidyl inositol-linked membrane protein, acts as a bone morphogenetic protein coreceptor to activate hepcidin expression through a SMAD signaling pathway in hepatocytes. In the present study, we show in mice that loss of hemojuvelin specifically in the liver leads to decreased liver hepcidin production and increased tissue and serum iron levels. Although it does not have any known function outside of the liver, hemojuvelin is expressed at very high levels in cardiac and skeletal muscle. To explore possible roles for hemojuvelin in skeletal muscle, we analyzed conditional knockout mice that lack muscle hemojuvelin. The mutant animals had no apparent phenotypic abnormalities. We found that systemic iron homeostasis and liver hepcidin expression were not affected by loss of hemojuvelin in skeletal muscle regardless of dietary iron content. We conclude that, in spite of its expression pattern, hemojuvelin is primarily important in the liver.

Full Text

Duke Authors

Cited Authors

  • Chen, W; Huang, FW; de Renshaw, TB; Andrews, NC

Published Date

  • June 9, 2011

Published In

Volume / Issue

  • 117 / 23

Start / End Page

  • 6319 - 6325

PubMed ID

  • 21493799

Pubmed Central ID

  • 21493799

Electronic International Standard Serial Number (EISSN)

  • 1528-0020

Digital Object Identifier (DOI)

  • 10.1182/blood-2010-12-327957

Language

  • eng

Conference Location

  • United States