PUBLICATION

Iron deficiency anemia's affect on bone formation in zebrafish mutant

Authors
Bo, L., Liu, Z., Zhong, Y., Huang, J., Chen, B., Wang, H., Xu, Y.
ID
ZDB-PUB-160519-28
Date
2016
Source
Biochemical and Biophysical Research Communications   475(3): 271-6 (Journal)
Registered Authors
Huang, Jian, Wang, Han, Zhong, Yingbin
Keywords
Bone formation, Fpn1, Iron deficiency anemia, Zebrafish
MeSH Terms
  • Anemia, Iron-Deficiency/complications
  • Anemia, Iron-Deficiency/genetics*
  • Anemia, Iron-Deficiency/metabolism
  • Anemia, Iron-Deficiency/physiopathology*
  • Animals
  • Bone Morphogenetic Proteins/metabolism
  • Bone and Bones/metabolism
  • Bone and Bones/physiopathology*
  • Cation Transport Proteins/genetics*
  • Disease Models, Animal
  • Gene Expression Regulation, Developmental
  • Mutation
  • Osteogenesis*
  • Signal Transduction
  • Zebrafish/genetics*
  • Zebrafish/physiology
  • Zebrafish Proteins/genetics*
PubMed
27184405 Full text @ Biochem. Biophys. Res. Commun.
Abstract
Iron is one of the essential elements of life. Iron metabolism is related to bone metabolism. Previous studies have confirmed that iron overload is a risk factor for osteoporosis. But the correlation between iron deficiency and bone metabolism remains unclear. Ferroportin 1 is identified as a cellular iron exporter and required for normal iron cycling. In human, the mutation in Ferroportin 1 gene caused hemochromatosis (iron overload) syndrome. In zebrafish, the mutant of ferroportin 1 gene (fpn1), Weh(tp85c) exhibited the defective iron transport, leading to developing severe hypochromic anemia. To understand the mechanism of fpn1 in iron regulation and bone formation, we used Weh(tp85c) as a model for investigating iron deficiency and bone metabolism. In this study, we examined the morphology of the developing cartilage and vertebrae of the Weh(tp85) compared to the wild type siblings by staining the larvae with alcian blue for cartilage and alizarin red for the bone. In addition, we evaluated the expression patterns of the marker genes of bone development and cell signaling in bone formation. Our results showed that weh(tp85c) mutant larvae exhibited the defects in bone formation, revealing by decreases in the number of calcified vertebrae along with decreased expression of osteoblast novel genes: alpl, runx2a and col1a1a and BMPs signaling genes in osteoblast differentiation: bmp2a and bmp2b. Our data suggest that iron deficiency anemia affects bone formation, potentially through the BMPs signaling pathway in zebrafish.
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Human Disease / Model
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