Corticosterone induces dysregulation of iron metabolism in hippocampal neurons in vitro

Lei Wang, Huanyu Wang, Li Li, Wei Li, Xiaoman Dong, Min Li, Li Lv*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

4 Scopus citations


Iron is required for neuronal function but in excess generates neurodegeneration. Although the iron homeostasis machinery in neurons has been described extensively, little is known about the influence of corticosterone on the iron homeostasis in neurons. In this study, we characterized the response of hippocampal neurons to a model of progressive corticosterone condition. We found that increasing extracellular corticosterone-induced iron accumulation killed a large proportion of neurons. Iron concentrations were significantly increased in the corticosterone-treated cells. In the hippocampal neurons, corticosterone decreased expression of ferritin and increased expression of transferrin receptor1 (TfR1), iron regulatory protein1 (IRP1), and divalent metal transporter 1. Corticosterone-induced elevation of IRP1 expression can cause increase of TfR1 and decrease of ferritin expression, which further leads to iron accumulation in hippocampal neurons and subsequently increases the oxidative damage of the neurons; it is indicated that corticosterone might be an important reason for iron deposition-caused neurodegenerative diseases.

Original languageEnglish (US)
Pages (from-to)88-95
Number of pages8
JournalBiological Trace Element Research
Issue number1
StatePublished - Oct 2010


  • Corticosterone
  • Hippocampal neuron
  • Iron homeostasis
  • Neurodegeneration

ASJC Scopus subject areas

  • Biochemistry, medical
  • Biochemistry
  • Clinical Biochemistry
  • Inorganic Chemistry
  • Endocrinology, Diabetes and Metabolism


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