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Iron plays essential roles in the central nervous system. However, how the iron level is regulated in brain cells including glia and neurons remains to be fully clarified. In this study, the localizations of hepcidin, ferroportin, and hephaestin, which are known to be involved in iron efflux, were immunohistochemically examined in autopsied human brains. Immunoreactivities for hepcidin and ferroportin were observed in granular structures within the cytoplasm of reactive astrocytes and epithelial cells of the choroid plexus. Granular structures showing immunoreactivities for hepcidin and ferroportin were also stained with antibodies for early endosome antigen 1 (EEA1). In addition, immunoreactivity for hephaestin was observed in the cytoplasm of epithelial cells of the choroid plexus as well as reactive astrocytes. Immunoreactivity for hephaestin in the cytoplasm of reactive astrocytes was occasionally colocalized with immunoreactivity for EEA1, while that of hephaestin was frequently observed in the cytoplasm showing no immunoreactivity for EEA1. These findings suggest that immunoreactivities for hepcidin and ferroportin are localized in close proximity to granular structures showing immunoreactivity for EEA1 in the cytoplasm of human brain astrocytes. They also suggest that immunoreactivity of hephaestin is localized in the cytoplasm of the choroid plexus epithelium as well as reactive astrocytes of human brains.
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http://dx.doi.org/10.1111/neup.12611 | DOI Listing |
Microorganisms
August 2025
Center for Hypertension and Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine and Life Sciences, Toledo, OH 43614, USA.
parasites rely on host iron for survival and replication, making host iron availability a critical determinant of malaria pathogenesis. Central to iron homeostasis is the hepcidin-ferroportin regulatory axis, where hepcidin suppresses iron export by inducing ferroportin degradation, thus modulating systemic and cellular iron availability. In the infection model (), we observed a significant downregulation of hepatic expression, accompanied by an increase in hepatic expression.
View Article and Find Full Text PDFRev Invest Clin
August 2025
Department of Pediatrics, The First Affiliated Hospital of Shihezi University, Shihezi 832008, China. Electronic address:
Background: Anemia of inflammation (AI) is a mild form of anemia. Vitamin D deficiency has been linked to an increased risk of AI. This study aims to investigate the potential molecular mechanisms underlying the protective role of vitamin D in AI.
View Article and Find Full Text PDFVitam Horm
August 2025
Ministry of Education Key Laboratory of Molecular and Cellular Biology, Hebei Key Laboratory of Animal Physiology, Biochemistry and Molecular Biology, Hebei Research Center of the Basic Discipline of Cell Biology, Hebei Collaborative Innovation Center for Eco-Environment, College of Life Sciences, H
Iron is an essential trace element that plays a crucial role in various biological processes, including oxygen transport, DNA synthesis and cell proliferation. Iron homeostasis is a critical biological equilibrium that involves the balance of iron absorption, utilization, storage and excretion. Iron is intricately linked to the pathophysiology of cancer.
View Article and Find Full Text PDFCrit Rev Food Sci Nutr
August 2025
Nutrition Institute, Rio de Janeiro State University, Rio de Janeiro, Brazil.
Iron is an essential micronutrient involved in key physiological processes, including oxygen transport and mitochondrial energy production. As humans lack a regulated excretory pathway for excess iron, systemic homeostasis depends on tightly controlled mechanisms of intestinal absorption, cellular storage, and recycling. Dysregulation of these processes may result in iron deficiency or overload, both associated with significant health implications.
View Article and Find Full Text PDFZhong Nan Da Xue Xue Bao Yi Xue Ban
April 2025
Division of Immunology, Hunan Normal University Health Science Center, Changsha 410013.
Objectives: Pain sensitization, as a core feature of neuropathic pain (NP), is closely associated with inflammatory imbalance within the central nervous system. To investigate the effects of intrathecal injection of noggin (NOG) on mechanical hypersensitivity, microglial (MG) activation and polarization, and iron metabolism in a spinal nerve ligation (SNL)-induced rat model of NP, and to explore the role of signal transducer and activator of transcription 3 (STAT3) in MG phenotypic transformation.
Methods: Sixty-six Sprague-Dawley (SD) rats were randomly divided into 3 groups: Sham, SNL, and SNL+NOG.