Role of hepcidin in murine brain iron metabolism
| Autor: | X.-J. Di, J. Li, L.-J. Fu, P. Yu, Z.-M. Qian, Xiang Lin Duan, S.-M. Wang, D. R. Crooks, T. A. Rouault, Yan Zhong Chang |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
medicine.medical_specialty
congenital hereditary and neonatal diseases and abnormalities Aging Iron Striatum Hippocampus Article Cellular and Molecular Neuroscience Mice Hepcidins Hepcidin Internal medicine hemic and lymphatic diseases medicine Animals Molecular Biology Cation Transport Proteins Cells Cultured Pharmacology Cerebral Cortex Neurons Messenger RNA Mice Inbred BALB C biology nutritional and metabolic diseases Brain Cell Biology Metabolism Hypoxia (medical) Rats Endocrinology medicine.anatomical_structure Cerebral cortex Cerebral ventricle biology.protein Molecular Medicine medicine.symptom Hormone Antimicrobial Cationic Peptides |
| Zdroj: | Cellular and molecular life sciences : CMLS. 67(1) |
| ISSN: | 1420-9071 |
| Popis: | Brain iron homeostasis is maintained by a balance of both iron uptake and release, and accumulating evidence has revealed that brain iron concentrations increase with aging. Hepcidin, an iron regulatory hormone produced by hepatocytes in response to inflammatory stimuli, iron, and hypoxia, has been shown to be the long-sought hormone responsible for the regulation of body iron balance and recycling in mammals. In this study, we report that hepcidin is widely expressed in the murine brain. In cerebral cortex, hippocampus and striatum, hepcidin mRNA levels increased with aging. Injection of hepcidin into the lateral cerebral ventricle resulted in decreased Fpn1 protein levels in cerebral cortex, hippocampus, and striatum. Additionally, treatment of primary cultured neurons with hepcidin caused decreased neuronal iron release and Fpn1 protein levels. Together, our data provide further evidence that hepcidin may be involved in the regulation of brain iron metabolism. |
| Databáze: | OpenAIRE |
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