Overexpression of the zinc transporter Zip14 increases non‐transferrin‐bound iron uptake in cells

Liuzzi, Juan P.; Aydemir, Fikret; Knutson, Mitchell D.; Cousins, Robert J.

doi:10.1096/fasebj.20.4.a131-d

Cited by 2 publications

(2 citation statements)

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“…In addition, AST impact OLG physiology through the release of soluble factors that favor oligodendroglial differentiation (Domingues et al, 2016), physical AST-OLG contact (Sakurai et al, 1998), and the expression of connexins that favor the myelination process and axonal metabolism (Lutz et al, 2009). may be at play in this animal model and postulate that Zip14, an alternative iron transporter also localized on the astrocytic plasma membrane (Aydemir & Cousins, 2018;Lane et al, 2010;Liuzzi et al, 2006;Qian et al, 2000), may be responsible for this compensation. Therefore, an alternative pathway may be thought to take part in KO mice, while a residual DMT1 function persists in our experimental model.…”

Section: Discussionmentioning

confidence: 92%

Iron deficiency in astrocytes alters cellular status and impacts on oligodendrocyte differentiation

Marcora,

Mattera,

Goñi

et al. 2024

J of Neuroscience Research

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Iron deficiency (ID) has been shown to affect central nervous system (CNS) development and induce hypomyelination. Previous work from our laboratory in a gestational ID model showed that both oligodendrocyte (OLG) and astrocyte (AST) maturation was impaired. To explore the contribution of AST iron to the myelination process, we generated an in vitro ID model by silencing divalent metal transporter 1 (DMT1) in AST (siDMT1 AST) or treating AST with Fe3+ chelator deferoxamine (DFX; DFX AST). siDMT1 AST showed no changes in proliferation but remained immature. Co‐cultures of oligodendrocyte precursors cells (OPC) with siDMT1 AST and OPC cultures incubated with siDMT1 AST‐conditioned media (ACM) rendered a reduction in OPC maturation. These findings correlated with a decrease in the expression of AST‐secreted factors IGF‐1, NRG‐1, and LIF, known to promote OPC differentiation. siDMT1 AST also displayed increased mitochondrial number and reduced mitochondrial size as compared to control cells. DFX AST also remained immature and DFX AST‐conditioned media also hampered OPC maturation in culture, in keeping with a decrease in the expression of AST‐secreted growth factors IGF‐1, NRG‐1, LIF, and CNTF. DFX AST mitochondrial morphology and number showed results similar to those observed in siDMT1 AST. In sum, our results show that ID, induced through two different methods, impacts AST maturation and mitochondrial functioning, which in turn hampers OPC differentiation.

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Section: Discussionmentioning

confidence: 92%

Iron deficiency in astrocytes alters cellular status and impacts on oligodendrocyte differentiation

Marcora,

Mattera,

Goñi

et al. 2024

J of Neuroscience Research

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“…Fe 3+ in the acidic endosomes is reduced to Fe 2+ under the action of prostate six transmembrane antigen protein 3 (STEAP3), and then transferred to the cytoplasm by divalent metal ion transporter 1 (DMT1, SLC11A2) or zinc transporter 8/14 (ZIP8/14), and introduced into the labile iron pool (LIP) (Bogdan et al, 2016). In addition, DMT1 and ZIP8/14 can also directly transport extracellular free Fe 2+ to intracellular LIP (Liuzzi et al, 2006;Wang et al, 2012). Excessive Fe 2+ in lip can produce a large amount of reactive oxygen species (ROS) through Fenton reaction, causing lipid peroxidation and cell death (Stockwell et al, 2017).…”

Section: Microrna Targeting Iron Metabolismmentioning

confidence: 99%

Relationship between miRNA and ferroptosis in tumors

Dai

Long

et al. 2022

Front. Pharmacol.

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Malignant tumor is a major killer that seriously endangers human health. At present, the methods of treating tumors include surgical resection, chemotherapy, radiotherapy and immunotherapy. However, the survival rate of patients is still very low due to the complicated mechanism of tumor occurrence and development and high recurrence rate. Individualized treatment will be the main direction of tumor treatment in the future. Because only by understanding the molecular mechanism of tumor development and differentially expressed genes can we carry out accurate treatment and improve the therapeutic effect. MicroRNA (miRNA) is a kind of small non coding RNA, which regulates gene expression at mRNA level and plays a key role in tumor regulation. Ferroptosis is a kind of programmed death caused by iron dependent lipid peroxidation, which is different from apoptosis, necrosis and other cell death modes. Now it has been found that ferroptosis plays an important role in the occurrence and development of tumors and drug resistance. More and more studies have found that miRNAs can regulate tumor development and drug resistance through ferroptosis. Therefore, in this review, the mechanism of ferroptosis is briefly outlined, and the relationship between miRNAs and ferroptosis in tumors is reviewed.

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Overexpression of the zinc transporter Zip14 increases non‐transferrin‐bound iron uptake in cells

Cited by 2 publications

References 0 publications

Iron deficiency in astrocytes alters cellular status and impacts on oligodendrocyte differentiation

Iron deficiency in astrocytes alters cellular status and impacts on oligodendrocyte differentiation

Relationship between miRNA and ferroptosis in tumors

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