Angiotensin II inhibits iron uptake and release in cultured neurons

Neurochem Res. 2014 May;39(5):893-900. doi: 10.1007/s11064-014-1285-3. Epub 2014 Mar 30.

Abstract

Based on the well-confirmed roles of angiotensin II (ANGII) in iron transport of peripheral organs and cells, the causative link of excess brain iron with and the involvement of ANGII in neurodegenerative disorders, we speculated that ANGII might also have an effect on expression of iron transport proteins in the brain. In the present study, we investigated effects of ANGII on iron uptake and release using the radio-isotope methods as well as expression of cell iron transport proteins by Western blot analysis in cultured neurons. Our findings demonstrated for the first time that ANGII significantly reduced transferrin-bound iron and non-transferrin bound iron uptake and iron release as well as expression of two major iron uptake proteins transferrin receptor 1 and divalent metal transporter 1 and the key iron exporter ferroportin 1 in cultured neurons. The findings suggested that endogenous ANGII might have a physiological significance in brain iron metabolism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiotensin II / pharmacology
  • Angiotensin II / physiology*
  • Animals
  • Antigens, CD / biosynthesis
  • Cation Transport Proteins / biosynthesis
  • Cells, Cultured
  • Iron / metabolism*
  • Iron Radioisotopes / metabolism
  • Male
  • Neurons / metabolism
  • Rats, Sprague-Dawley
  • Receptors, Transferrin / biosynthesis
  • Transferrin / metabolism*

Substances

  • Antigens, CD
  • CD71 antigen
  • Cation Transport Proteins
  • Iron Radioisotopes
  • Receptors, Transferrin
  • Transferrin
  • metal transporting protein 1
  • solute carrier family 11- (proton-coupled divalent metal ion transporters), member 2
  • Angiotensin II
  • Iron