ArticleFree radical biology & medicine2012
PPARδ prevents radiation-induced proinflammatory responses in microglia via transrepression of NF-κB and inhibition of the PKCα/MEK1/2/ERK1/2/AP-1 pathway.
Article in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 87 citations in OpenAlex.
- Pharmacological Targeting of Peroxisome Proliferator-activated Receptors for Prevention of Radiation-induced Cognitive Decline.Annals of neurosciences · 2026Review
- The CEBPB-AP-1 (JunB/Fos) Axis Drives Neuroinflammation and Microglial Dysfunction Via TNF Signaling in Ischemic Stroke.Inflammation · 2026Article
- Cannabidiol and other non-psychotropic cannabinoids from Cannabis sativa as therapeutics for microglial-mediated neuroinflammation and neurodegeneration.Journal of cannabis research · 2026Review
- Dose-Dependent Dual Effects of Gradient Ionizing Radiation on Neurocognition.International journal of molecular sciences · 2026Review
- Radiation-Induced Neurodegeneration.Biomedicines · 2026Review
- Radiation-induced Brain Injury and the Radiation Late Effects Cohort (RLEC) of Rhesus Macaques (Macaca mulatta).Radiation research · 2025Review
- Central Nervous System Response Against Ionizing Radiation Exposure: Cellular, Biochemical, and Molecular Perspectives.Molecular neurobiology · 2025Review
- Quantitative proteomic analysis reveals key proteins involved in radiation-induced brain injury.PloS one · 2025Article
- Neurodegenerative diseases and neuroinflammation-induced apoptosis.Open life sciences · 2025Review
- Hyperbaric oxygen therapy attenuates brain radiation-induced cognitive deficits in rats.International journal of medical sciences · 2025Article
- Peroxisome Proliferator-Activated Receptor δ Suppresses the Cytotoxicity of CD8+ T Cells by Inhibiting RelA DNA-Binding Activity.Cancer research communications · 2024Article
- Microglia in radiation-induced brain injury: Cellular and molecular mechanisms and therapeutic potential.CNS neuroscience & therapeutics · 2024Review
- Galactic Cosmic Ray Particle Exposure Does Not Increase Protein Levels of Inflammation or Oxidative Stress Markers in Rat Microglial Cells In Vitro.International journal of molecular sciences · 2024Article
- IFN-γ promotes radioresistant Nestin-expressing progenitor regeneration in the developing cerebellum by augmenting Shh ligand production.CNS neuroscience & therapeutics · 2024Article
- Reprimo (RPRM) as a Potential Preventive and Therapeutic Target for Radiation-Induced Brain Injury via Multiple Mechanisms.International journal of molecular sciences · 2023Article
- Advances in the study of the molecular biological mechanisms of radiation-induced brain injury.American journal of cancer research · 2023Review
- Microglia as Therapeutic Target for Radiation-Induced Brain Injury.International journal of molecular sciences · 2022Review
- Review
- Flavonoids, the Family of Plant-Derived Antioxidants Making Inroads into Novel Therapeutic Design Against Ionizing Radiation-Induced Oxidative Stress in Parkinson's Disease.Current neuropharmacology · 2022Review
- Ionizing radiation, cerebrovascular disease, and consequent dementia: A review and proposed framework relevant to space radiation exposure.Frontiers in physiology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Partial or whole-brain irradiation is often required to treat both primary and metastatic brain cancer. Radiation-induced normal tissue injury, including progressive cognitive impairment, however, can significantly affect the well-being of the approximately 200,000 patients who receive these treatments each year in the United States. Although the exact mechanisms underlying radiation-induced late effects remain unclear, oxidative stress and inflammation are thought to play a critical role. Microglia are key mediators of neuroinflammation. Peroxisomal proliferator-activated receptor (PPAR) δ has been shown to be a potent regulator of anti-inflammatory responses. Thus, we hypothesized that PPARδ activation would modulate the radiation-induced inflammatory response in microglia. Incubating BV-2 murine microglial cells with the PPARδ agonist L-165041 prevented the radiation-induced increase in: (i) intracellular reactive oxygen species generation, (ii) Cox-2 and MCP-1 expression, and (iii) IL-1β and TNF-α message levels. This occurred, in part, through PPARδ-mediated modulation of stress-activated kinases and proinflammatory transcription factors. PPARδ inhibited NF-κB via transrepression by physically interacting with the p65 subunit and prevented activation of the PKCα/MEK1/2/ERK1/2/AP-1 pathway by inhibiting the radiation-induced increase in intracellular reactive oxygen species generation. These data support the hypothesis that PPARδ activation can modulate radiation-induced oxidative stress and inflammatory responses in microglia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.