The total iron level in the brain increases with age, and excess iron is associated with neurodegenerative diseases; however, the mechanism of brain iron deposition is unknown. In peripheral cells, the expression of hepcidin, a master regulator of iron homeostasis, is regulated by estrogen. This study aimed to determine whether hepcidin was involved in iron deposition in the brain and brain endothelial cells of estrogen-deficient aged female mice. Aged mice showed increased levels of hepcidin and ferritin in the brain and brain microvessels compared with young mice, and these levels were reduced by estrogen replacement in ovariectomized aged mice. In the brain endothelial cell line bEnd.3, the lipopolysaccharide (10 ng/mL)-induced increases of hepcidin mRNA and protein levels, the number of Prussian blue–positive cells, and free radicals were reduced after estrogen treatment. These results suggest that estrogen deficiency with an increase of hepcidin is partly responsible for iron deposition in the brain and brain endothelial cells and that hepcidin can be a target to prevent brain aging and neurodegeneration in postmenopausal women.
|Number of pages||10|
|Journal||Neurobiology of Aging|
|State||Published - Dec 2020|
Bibliographical noteFunding Information:
This work was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF), South Korea grant funded by the Ministry of Education , South Korea ( NRF-2015R1C1A1A01052593 ) and by the Korea government ( MSIT ), South Korea ( NRF-2019R1A2C1087035 and NRF-2020R1A5A2019210 ).
© 2020 Elsevier Inc.
- Brain endothelial cell
- Iron accumulation