Vitamin D3 alters microglia immune activation by an IL-10 dependent SOCS3 mechanism

Boontanrart, Mandy; Hall, Samuel D.; Spanier, Justin A.; Hayes, Colleen E.; Olson, Julie K.

doi:10.1016/j.jneuroim.2016.01.015

Cited by 97 publications

(70 citation statements)

References 54 publications

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“…Indeed, prophylactic vitamin D3 has improved dopaminergic neuronal survival significantly in an MPTP model of PD through suppression of microglial activation (63). As suggested, vitamin D3 elevates microglial IL-10 expression; inducing suppressor of cytokine signaling-3, leading to a decline in pro-inflammatory cytokines expression in microglia (64). …”

Section: Riboflavin Ameliorates Oxidative Stress Mitochondrial Dysfumentioning

confidence: 96%

Riboflavin Has Neuroprotective Potential: Focus on Parkinson’s Disease and Migraine

Marashly

Bohlega

2017

Front. Neurol.

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With the huge negative impact of neurological disorders on patient’s life and society resources, the discovery of neuroprotective agents is critical and cost-effective. Neuroprotective agents can prevent and/or modify the course of neurological disorders. Despite being underestimated, riboflavin offers neuroprotective mechanisms. Significant pathogenesis-related mechanisms are shared by, but not restricted to, Parkinson’s disease (PD) and migraine headache. Those pathogenesis-related mechanisms can be tackled through riboflavin proposed neuroprotective mechanisms. In fact, it has been found that riboflavin ameliorates oxidative stress, mitochondrial dysfunction, neuroinflammation, and glutamate excitotoxicity; all of which take part in the pathogenesis of PD, migraine headache, and other neurological disorders. In addition, riboflavin-dependent enzymes have essential roles in pyridoxine activation, tryptophan-kynurenine pathway, and homocysteine metabolism. Indeed, pyridoxal phosphate, the active form of pyridoxine, has been found to have independent neuroprotective potential. Also, the produced kynurenines influence glutamate receptors and its consequent excitotoxicity. In addition, methylenetetrahydrofolate reductase requires riboflavin to ensure normal folate cycle influencing the methylation cycle and consequently homocysteine levels which have its own negative neurovascular consequences if accumulated. In conclusion, riboflavin is a potential neuroprotective agent affecting a wide range of neurological disorders exemplified by PD, a disorder of neurodegeneration, and migraine headache, a disorder of pain. In this article, we will emphasize the role of riboflavin in neuroprotection elaborating on its proposed neuroprotective mechanisms in opposite to the pathogenesis-related mechanisms involved in two common neurological disorders, PD and migraine headache, as well as, we encourage the clinical evaluation of riboflavin in PD and migraine headache patients in the future.

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Section: Riboflavin Ameliorates Oxidative Stress Mitochondrial Dysfumentioning

confidence: 96%

Riboflavin Has Neuroprotective Potential: Focus on Parkinson’s Disease and Migraine

Marashly

Bohlega

2017

Front. Neurol.

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“…Vitamin D is an active neuro-steroid, believed to modulate pro-inflammatory cytokine release from microglia 51,52). Despite being seemingly one of the most studied supplemental treatment for ASD, studies targeting use of vitamin D as a treatment or prophylaxis for ASD; however, have been yielding mixed results.…”

Section: Immunomodulatory Treatmentmentioning

confidence: 99%

Microglia and Autism Spectrum Disorder: Overview of Current Evidence and Novel Immunomodulatory Treatment Options

Kim

Hong

Bae

2018

Clin Psychopharmacol Neurosci

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Autism spectrum disorder is a rapidly increasing heterogeneous neurodevelopmental syndrome, remarked by persistent deficit in social communication, and restricted, repetitive patterns of behavior and interest. Lately, maternal immune activation and micgroglial dysfunction in the developing brain have been gaining mounting evidence and leading to studies of various novel agents as potential treatment options. A few immunomodulatory treatment options—luteolin, minocycline, suramin, vitamin D, gut microbiota—are discussed in the current article, regarding the current understanding of their mechanisms and evidence for potential clinical use. More studies are warranted to understand their exact mechanisms of action and to verify efficacy and safety in human subjects.

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“…Therefore, how to overcome DDP resistance will be a key issue for the design of more effective individualized therapeutic strategies. SOCS 3, one of the best characterized molecules of the SOCS family, functions as an important role in immune and inflammatory processes [13,14]. However, the study regarding the relationship between activation of SOCS 3 and the sensitivity of DDP has been not reported.…”

Section: Discussionmentioning

confidence: 99%

Interferon-γ Upregulates SOCS3 Expression to Reduce Cisplatin Chemoresistance in Non-Small Cell Lung Cancer A549 Cells

Xu¹,

Tang²,

Gong³

et al. 2016

Chemotherapy

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Background: Cisplatin (DDP)-based chemotherapy is the mainstay of first-line therapeutic strategy for the treatment of advanced non-small cell carcinoma (NSCLC). However, the anticancer efficacy of DDP is often limited by the existence or development of chemoresistance. Thus, we investigated the effect of interferon-γ on DDPresistant A549 cell. Methods: Semi-quantitative RT-PCR was used to compare the differences of SOCS3 mRNA expression in both cisplatin-resistant A549 (A549/DDP) cell and the parental A549 cell. The cellular sensitivity to cisplatin, cell viability and apoptosis were detected by MTT, flow cytometry and Western blotting. Results: Semi-quantitative RT-PCR and western blotting showed that SOCS 3 expression was significantly down-regulated in A549/DDP cell compared to the parental A549 and normal human bronchial epithelial cells BEAS-2B. IFN-γ treatment could restore SOCS3 expression, resulting in an increased sensitivity of these resistant A549 cells to DDP. In addition, p53 and Bcl-2 signaling pathways were also involved in regulating IFN-γ-induced cell death in DDP-resistant A549 cells. Conclusion: Our study indicates that SOCS 3 may play a crucial role in the progress of cisplatin resistance of A549. Moreover, IFN-γ could induce SOCS3 expression and potentiate the re-sensitization of these resistant A549 cells to DDP.

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Vitamin D3 alters microglia immune activation by an IL-10 dependent SOCS3 mechanism

Cited by 97 publications

References 54 publications

Riboflavin Has Neuroprotective Potential: Focus on Parkinson’s Disease and Migraine

Riboflavin Has Neuroprotective Potential: Focus on Parkinson’s Disease and Migraine

Microglia and Autism Spectrum Disorder: Overview of Current Evidence and Novel Immunomodulatory Treatment Options

Interferon-γ Upregulates SOCS3 Expression to Reduce Cisplatin Chemoresistance in Non-Small Cell Lung Cancer A549 Cells

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