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Cells
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Regulation of Iron Metabolism in Health and Disease
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Regulation of Iron Metabolism in Health and Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 4761

Special Issue Editor

Dr. Jaya Gnana-Prakasam

E-Mail Website
Guest Editor
Department of Ophthalmology, Department of Biochemistry and Molecular Biology, Saint Louis University, St. Louis, MO, USA
Interests: iron metabolism; diabetes; inflammation

Special Issue Information

Dear Colleagues,

Iron is an essential nutrient necessary for the function of critical proteins involved in biochemical reactions that are indispensable for normal cellular function. However, excess iron is toxic to cells as they undergo the Fenton reaction, catalyzing the production of reactive oxygen species and leading to tissue damage. Due to the lack of specific excretory mechanisms, iron is progressively accrued with aging. Genetic factors and excess dietary iron intake may contribute further to intracellular iron accumulation. Recent evidence links several chronic disorders to deregulated iron homeostasis. Iron’s contributory role in disease pathogenesis has been identified not only in genetic disorders of iron overload but also in cancer, diabetes, cardiovascular diseases, endocrine dysfunction, neurodegenerative diseases and ocular disorders. Thus, reducing intracellular iron levels is a promising therapeutic target for these diseases. Siderophores and synthetic iron chelators are currently in clinical use to decrease iron levels. However, there are challenges in developing novel and safe iron chelators that specifically target individual organs. Current therapeutic targets under study include BMP/Smad signaling, hepcidin–ferroportin axis, Wnt signaling, oxidative stress pathways, inflammasome signaling, ferritinophagy and ferroptosis. This Special Issue welcomes submission of original research articles, reviews, clinical trials and brief reports related to the role of iron metabolism in disease pathogenesis and the elucidation of novel therapeutic agents that target these molecular pathways.

Dr. Jaya Gnana-Prakasam
Guest Editor

Manuscript Submission Information

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Keywords

  • iron metabolism
  • oxidative stress
  • inflammation
  • ferroptosis
  • ferritinophagy
  • hepcidin
  • iron chelators
  • neurodegeneration
  • cardiovascular
  • cancer

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Published Papers (3 papers)

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Research

17 pages, 9072 KiB  
Article
Upregulation of Transferrin Receptor 1 (TfR1) but Not Glucose Transporter 1 (GLUT1) or CD98hc at the Blood–Brain Barrier in Response to Valproic Acid
by Steinunn Sara Helgudóttir, Kasper Bendix Johnsen, Lisa Greve Routhe, Charlotte Laurfelt Munch Rasmussen, Maj Schneider Thomsen and Torben Moos
Cells 2024, 13(14), 1181; https://doi.org/10.3390/cells13141181 - 11 Jul 2024
Viewed by 1103
Abstract
Background: Transferrin receptor 1 (TfR1), glucose transporter 1 (GLUT1), and CD98hc are candidates for targeted therapy at the blood–brain barrier (BBB). Our objective was to challenge the expression of TfR1, GLUT1, and CD98hc in brain capillaries using the histone deacetylase inhibitor (HDACi) valproic [...] Read more.
Background: Transferrin receptor 1 (TfR1), glucose transporter 1 (GLUT1), and CD98hc are candidates for targeted therapy at the blood–brain barrier (BBB). Our objective was to challenge the expression of TfR1, GLUT1, and CD98hc in brain capillaries using the histone deacetylase inhibitor (HDACi) valproic acid (VPA). Methods: Primary mouse brain capillary endothelial cells (BCECs) and brain capillaries isolated from mice injected intraperitoneally with VPA were examined using RT-qPCR and ELISA. Targeting to the BBB was performed by injecting monoclonal anti-TfR1 (Ri7217)-conjugated gold nanoparticles measured using ICP-MS. Results: In BCECs co-cultured with glial cells, Tfrc mRNA expression was significantly higher after 6 h VPA, returning to baseline after 24 h. In vivo Glut1 mRNA expression was significantly higher in males, but not females, receiving VPA, whereas Cd98hc mRNA expression was unaffected by VPA. TfR1 increased significantly in vivo after VPA, whereas GLUT1 and CD98hc were unchanged. The uptake of anti-TfR1-conjugated nanoparticles was unaltered by VPA despite upregulated TfR expression. Conclusions: VPA upregulates TfR1 in brain endothelium in vivo and in vitro. VPA does not increase GLUT1 and CD98hc proteins. The increase in TfR1 does not result in higher anti-TfR1 antibody targetability, suggesting targeting sufficiently occurs with available transferrin receptors without further contribution from accessory VPA-induced TfR1. Full article
(This article belongs to the Special Issue Regulation of Iron Metabolism in Health and Disease)
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17 pages, 9991 KiB  
Article
Iron Regulates Cellular Proliferation by Enhancing the Expression of Glucose Transporter GLUT3 in the Liver
by Kleber S. Ribeiro, Eshani Karmakar, Christine Park, Richa Garg, George P. Kung, Isha Kadakia, Jyotsna S. Gopianand, Tejas Arun, Oleg Kisselev and Jaya P. Gnana-Prakasam
Cells 2024, 13(13), 1147; https://doi.org/10.3390/cells13131147 - 4 Jul 2024
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Abstract
Iron is often accumulated in the liver during pathological conditions such as cirrhosis and cancer. Elevated expression of glucose transporters GLUT1 and GLUT3 is associated with reduced overall survival in patients with hepatocellular carcinoma. However, it is not known whether iron can regulate [...] Read more.
Iron is often accumulated in the liver during pathological conditions such as cirrhosis and cancer. Elevated expression of glucose transporters GLUT1 and GLUT3 is associated with reduced overall survival in patients with hepatocellular carcinoma. However, it is not known whether iron can regulate glucose transporters and contribute to tumor proliferation. In the present study, we found that treatment of human liver cell line HepG2 with ferric ammonium citrate (FAC) resulted in a significant upregulation of GLUT3 mRNA and protein in a dose-dependent manner. Similarly, iron accumulation in mice fed with high dietary iron as well as in mice injected intraperitoneally with iron dextran enhanced the GLUT3 expression drastically in the liver. We demonstrated that iron-induced hepatic GLUT3 upregulation is mediated by the LKB1/AMPK/CREB1 pathway, and this activation was reversed when treated with iron chelator deferiprone. In addition, inhibition of GLUT3 using siRNA prevented iron-mediated increase in the expression of cell cycle markers and cellular hyperproliferation. Furthermore, exogenous sodium beta-hydroxybutyrate treatment prevented iron-mediated hepatic GLUT3 activation both in vitro and in vivo. Together, these results underscore the importance of iron, AMPK, CREB1 and GLUT3 pathways in cell proliferation and highlight the therapeutic potential of sodium beta-hydroxybutyrate in hepatocellular carcinoma with high GLUT3 expression. Full article
(This article belongs to the Special Issue Regulation of Iron Metabolism in Health and Disease)
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15 pages, 5614 KiB  
Article
Ferritin Is Secreted from Primary Cultured Astrocyte in Response to Iron Treatment via TRPML1-Mediated Exocytosis
by Xiaoqi Yu, Zhixin Xiao, Junxia Xie and Huamin Xu
Cells 2023, 12(21), 2519; https://doi.org/10.3390/cells12212519 - 25 Oct 2023
Cited by 1 | Viewed by 1708
Abstract
Impaired iron homeostasis has been proven to be one of the critical contributors to the pathology of Parkinson’s disease (PD). Ferritin is considered an intracellular protein responsible for storing cytosolic iron. Recent studies have found that ferritin can be secreted from cells independent [...] Read more.
Impaired iron homeostasis has been proven to be one of the critical contributors to the pathology of Parkinson’s disease (PD). Ferritin is considered an intracellular protein responsible for storing cytosolic iron. Recent studies have found that ferritin can be secreted from cells independent of the classical endoplasmic reticulum–Golgi system. However, the precise mechanisms underlying the secretion of ferritin in the brain were not elucidated. In the present study, we demonstrated that the primary cultured astrocytes do have the ability to secrete ferritin, which is enhanced by iron treatment. Increased ferritin secretion was accompanied by increased protein expression of ferritin response to iron stimulation. Further study showed that iron-induced expression and secretion of ferritin could be inhibited by CQ or 3-MA pretreatment. In addition, the knockdown of transient receptor potential mucolipin 1 (TRPML1) antagonized iron-induced ferritin secretion, accompanied by further increased intracellular protein levels of ferritin. Further study demonstrated that ferritin colocalized with LAMP1 in iron-treated astrocytes. On the contrary, ras-associated protein 27a (Rab27a) knockdown further enhanced iron-induced ferritin secretion and decreased intracellular protein levels of ferritin. Furthermore, we also showed that the secretory autophagy protein tripartite motif containing 16 (TRIM16) and sec22b decreased in iron-treated astrocytes. These results suggested that astrocytes might secrete ferritin via TRPML1-mediated exocytosis. This provides new evidence for the mechanisms underlying the secretion of ferritin in primary cultured astrocytes under a high iron environment. Full article
(This article belongs to the Special Issue Regulation of Iron Metabolism in Health and Disease)
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