ArticleJournal of neurochemistry2012
Modulation of interferon-γ-induced glial cell activation by transforming growth factor β1: a role for STAT1 and MAPK pathways.
Article in Journal of neurochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
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- Age-dependent changes on fractalkine forms and their contribution to neurodegenerative diseases.Frontiers in molecular neuroscience · 2023Review
- Garden Cress (Neuropsychiatric disease and treatment · 2023Article
- NOX2 Activation in COVID-19: Possible Implications for Neurodegenerative Diseases.Medicina (Kaunas, Lithuania) · 2021Review
- MAPK signaling determines lysophosphatidic acid (LPA)-induced inflammation in microglia.Journal of neuroinflammation · 2020Article
- Small-Molecule Lysophosphatidic Acid Receptor 5 (LPAR5) Antagonists: Versatile Pharmacological Tools to Regulate Inflammatory Signaling in BV-2 Microglia Cells.Frontiers in cellular neuroscience · 2019Article
- The Role of NADPH Oxidases and Oxidative Stress in Neurodegenerative Disorders.International journal of molecular sciences · 2018Review
- Physical interaction of STAT1 isoforms with TGF-β receptors leads to functional crosstalk between two signaling pathways in epithelial ovarian cancer.Journal of experimental & clinical cancer research : CR · 2018Article
- Tetrahydroxystilbene Glucoside Produces Neuroprotection against 6-OHDA-Induced Dopamine Neurotoxicity.Oxidative medicine and cellular longevity · 2018Article
- Computational Investigation of Ginsenoside F1 fromIranian journal of pharmaceutical research : IJPR · 2018Article
- Expression of Tgfβ1 and Inflammatory Markers in the 6-hydroxydopamine Mouse Model of Parkinson's Disease.Frontiers in molecular neuroscience · 2016Article
- Role of TGFβ signaling in the pathogenesis of Alzheimer's disease.Frontiers in cellular neuroscience · 2015Article
- Mitogen-Activated Protein Kinase Phosphatase (MKP)-1 in Nervous System Development and Disease.Molecular neurobiology · 2015Review
- Microglial cell dysregulation in brain aging and neurodegeneration.Frontiers in aging neuroscience · 2015Review
- Neuroinflammation: good, bad, or indifferent?Journal of neurochemistry · 2014Article
- Structure of excitatory synapses and GABAA receptor localization at inhibitory synapses are regulated by neuroplastin-65.The Journal of biological chemistry · 2014Article
- Age-dependent changes on TGFβ1 Smad3 pathway modify the pattern of microglial cell activation.Brain, behavior, and immunity · 2014Article
- Magnolia polyphenols attenuate oxidative and inflammatory responses in neurons and microglial cells.Journal of neuroinflammation · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Overactivated glial cells can produce neurotoxic oxidant molecules such as nitric oxide (NO·) and superoxide anion (O(2)·(-)). We have previously reported that transforming growth factor β1 (TGFβ1) released by hippocampal cells modulates interferon-γ (IFNγ)-induced production of O(2)·(-) and NO· by glial cells. However, underlying molecular mechanisms are not completely understood, thereby, the aim of this work was to study the effect of TGFβ1 on IFNγ-induced signaling pathways. We found that costimulation with TGFβ1 decreased IFNγ-induced phosphorylation of signal transducer and activator of transcription-type-1 (STAT1) and extracellular signal-regulated kinase (ERK), which correlated with a reduced O(2)·(-) and NO· production in mixed and purified glial cultures. Moreover, IFNγ caused a decrease in TGFβ1-mediated phosphorylation of P38, whereas pre-treatment with ERK and P38 inhibitors decreased IFNγ-induced phosphorylation of STAT1 on serine727 and production of radical species. These results suggested that modulation of glial activation by TGFβ1 is mediated by deactivation of MAPKs. Notably, TGFβ1 increased the levels of MAPK phosphatase-1 (MKP-1), whose participation in TGFβ1-mediated modulation was confirmed by MKP-1 siRNA transfection in mixed and purified glial cultures. Our results indicate that the cross-talk between IFNγ and TGFβ1 might regulate the activation of glial cells and that TGFβ1 modulated IFNγ-induced production of neurotoxic oxidant molecules through STAT1, ERK, and P38 pathways.
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