{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["64"],"submitter":["Ma J"],"pubmed_abstract":["<h4>Background</h4>Apolipoprotein E deficiency (ApoE<sup>-/-</sup>) increases progressively iron in the liver, spleen and aortic tissues with age in mice. However, it is unknown whether ApoE affects brain iron.<h4>Methods</h4>We investigated iron contents, expression of transferrin receptor 1 (TfR1), ferroportin 1 (Fpn1), iron regulatory proteins (IRPs), aconitase, hepcidin, Aβ42, MAP2, reactive oxygen species (ROS), cytokines and glutathione peroxidase 4 (Gpx4) in the brain of ApoE<sup>-/-</sup> mice.<h4>Results</h4>We demonstrated that ApoE<sup>-/-</sup> induced a significant increase in iron, TfR1 and IRPs and a reduction in Fpn1, aconitase and hepcidin in the hippocampus and basal ganglia. We also showed that replenishment of ApoE absent partly reversed the iron-related phenotype in Ap"],"journal":["Redox biology"],"pagination":["102779"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10363452"],"repository":["biostudies-literature"],"pubmed_title":["Apolipoprotein E is required for brain iron homeostasis in mice."],"pmcid":["PMC10363452"],"pubmed_authors":["Li W","Qian ZM","Zhong QX","Shen MQ","Ma J","Guo Q"],"additional_accession":[]},"is_claimable":false,"name":"Apolipoprotein E is required for brain iron homeostasis in mice.","description":"<h4>Background</h4>Apolipoprotein E deficiency (ApoE<sup>-/-</sup>) increases progressively iron in the liver, spleen and aortic tissues with age in mice. However, it is unknown whether ApoE affects brain iron.<h4>Methods</h4>We investigated iron contents, expression of transferrin receptor 1 (TfR1), ferroportin 1 (Fpn1), iron regulatory proteins (IRPs), aconitase, hepcidin, Aβ42, MAP2, reactive oxygen species (ROS), cytokines and glutathione peroxidase 4 (Gpx4) in the brain of ApoE<sup>-/-</sup> mice.<h4>Results</h4>We demonstrated that ApoE<sup>-/-</sup> induced a significant increase in iron, TfR1 and IRPs and a reduction in Fpn1, aconitase and hepcidin in the hippocampus and basal ganglia. We also showed that replenishment of ApoE absent partly reversed the iron-related phenotype in Ap","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Aug","modification":"2025-04-05T12:35:41.604Z","creation":"2025-04-05T12:35:41.604Z"},"accession":"S-EPMC10363452","cross_references":{"pubmed":["37339558"],"doi":["10.1016/j.redox.2023.102779"]}}