ArticleCellular and molecular neurobiology2019
Fractalkine Induces Hepcidin Expression of BV-2 Microglia and Causes Iron Accumulation in SH-SY5Y Cells.
Article in Cellular and molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
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- Stress-Induced Dysregulation of Brain Iron Metabolism and Its Links to Neurological Disorders.Biology · 2025Review
- The role of microglia in neurodegenerative diseases: from the perspective of ferroptosis.Acta pharmacologica Sinica · 2025Review
- Prostaglandin endoperoxide synthase 2 regulates neuroinflammation to mediate postoperative cognitive dysfunction in mice.Scientific reports · 2025Article
- Role of the CX3CL1/CX3CR1 axis in iron metabolism and immune regulation during acuteFrontiers in immunology · 2025Article
- Microglial-specific knockdown of iron import gene, Slc11a2, blunts LPS-induced neuroinflammatory responses in a sex-specific manner.Brain, behavior, and immunity · 2024Article
- Interplay of Vitamin D, Unfolded Protein Response, and Iron Metabolism in Neuroblastoma Cells: A Therapeutic Approach in Neurodegenerative Conditions.International journal of molecular sciences · 2023Article
- The Role of Fractalkine in the Regulation of Endometrial Iron Metabolism in Iron Deficiency.International journal of molecular sciences · 2023Article
- Ferroptosis and mitochondrial dysfunction in acute central nervous system injury.Frontiers in cellular neuroscience · 2023Review
- Astrocytes Reduce Store-Operated CaPharmaceuticals (Basel, Switzerland) · 2022Article
- Alterations of the expression levels of glucose, inflammation, and iron metabolism related miRNAs and their target genes in the hypothalamus of STZ-induced rat diabetes model.Diabetology & metabolic syndrome · 2022Article
- Modulatory Effects of Fractalkine on Inflammatory Response and Iron Metabolism of Lipopolysaccharide and Lipoteichoic Acid-Activated THP-1 Macrophages.International journal of molecular sciences · 2022Article
- The Role of Microglia in Alzheimer's Disease From the Perspective of Immune Inflammation and Iron Metabolism.Frontiers in aging neuroscience · 2022Review
- CX3CL1 Derived from Bone Marrow Mesenchymal Stem Cells Inhibits AComputational and mathematical methods in medicine · 2022Article
- Expression of antimicrobial host defence peptides in the central nervous system during health and disease.Discovery immunology · 2022Review
- Immunomodulatory and Antiprotozoal Potential of FabricatedPolymers · 2021Article
- Three chemotypes of thyme (Thymus vulgaris L.) essential oil and their main compounds affect differently the IL-6 and TNFα cytokine secretions of BV-2 microglia by modulating the NF-κB and C/EBPβ signalling pathways.BMC complementary medicine and therapies · 2021Article
- IL-6 Regulates Hepcidin Expression Via the BMP/SMAD Pathway by Altering BMP6, TMPRSS6 and TfR2 Expressions at Normal and Inflammatory Conditions in BV2 Microglia.Neurochemical research · 2021Article
- Distinct Effects ofInternational journal of molecular sciences · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
Fractalkine (CX3CL1) is a potent inflammatory mediator of the central nervous system, which is expressed by neurons and regulates microglial functions by binding to fractalkine receptor (CX3CR1). It has been demonstrated that neuroinflammation plays an important role in iron accumulation of the brain leading to neuronal cell death. The major regulator of iron homeostasis is the peptide hormone hepcidin. Hepcidin expression is triggered by inflammatory conditions, which may contribute to the neuronal iron accumulation. In the present study, we established a bilaminar co-culture system of differentiated SH-SY5Y cells and BV-2 microglia as a neuronal model to examine the effect of soluble fractalkine on iron homeostasis of microglia and SH-SY5Y cells. We determined the hepcidin expression of fractalkine-treated microglia which showed significant elevation. We examined the relation between increased hepcidin secretion, the known hepcidin regulators and the signalling pathways controlled by fractalkine receptor. Our data revealed that TMPRSS6 and alpha 1-antitrypsin levels decreased due to fractalkine treatment, as well as the activity of NFκB pathway and the tyrosine phosphorylation of STAT5 factor. Moreover, fractalkine-induced hepcidin production of microglia initiated ferroportin internalisation of SH-SY5Y cells, which contributed to iron accumulation of neurons. Our results demonstrate that soluble form of fractalkine regulates hepcidin expression of BV-2 cells through fractalkine-mediated CX3CR1 internalisation. Moreover, fractalkine indirectly contributes to the iron accumulation of SH-SY5Y cells by activating ferroportin internalisation and by triggering the expressions of divalent metal transporter-1, ferritin heavy chain and mitochondrial ferritin.
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