ArticleJournal of neuroinflammation2019
Epigenetic suppression of liver X receptor β in anterior cingulate cortex by HDAC5 drives CFA-induced chronic inflammatory pain.
Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Article
- Epigenetic, neuroplasticity, and adrenergic targets associated with major depression in immune cells.Scientific reports · 2026Article
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- The characteristics of brain function alterations in patients with chronic prostatitis/chronic pelvic pain syndrome across varying symptom severities evaluated by NIH-CPSI.Frontiers in neuroscience · 2025Article
- CCL2 Potentiates Inflammation Pain and Related Anxiety-Like Behavior Through NMDA Signaling in Anterior Cingulate Cortex.Molecular neurobiology · 2024Article
- Cholesterol-dependent LXR transcription factor activity represses pronociceptive effects of estrogen in sensory neurons and pain induced by myelin basic protein fragments.Brain, behavior, & immunity - health · 2024Article
- Linderane Attenuates Complete Freund's Adjuvant-Induced Pain and Anxiety in Mice by Restoring Anterior Cingulate Cortex Microglia M2 Polarization through Activating Cannabinoid 2 Receptor.ACS pharmacology & translational science · 2024Article
- Activation of LXRs alleviates neuropathic pain-induced cognitive dysfunction by modulation of microglia polarization and synaptic plasticity via PI3K/AKT pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- TRPA1 Ion Channel Mediates the Analgesic Effects of Acupuncture at the ST36 Acupoint in Mice Suffering from Arthritis.Journal of inflammation research · 2024Article
- Role of histone deacetylases in neuroplasticity impairments and inflammation in major depression.Neuroscience applied · 2024Review
- Rab11a in the spinal cord: an essential contributor to complete Freund's adjuvant-induced inflammatory pain in mice.Molecular brain · 2023Article
- Activation of the Hippocampal LXRβ Improves Sleep-Deprived Cognitive Impairment by Inhibiting Neuroinflammation.Molecular neurobiology · 2021Article
- Changes in the anterior cingulate cortex in Crohn's disease: A neuroimaging perspective.Brain and behavior · 2021Review
- Paeonol ameliorates CFA-induced inflammatory pain by inhibiting HMGB1/TLR4/NF-κB p65 pathway.Metabolic brain disease · 2021Article
- Electroacupuncture Regulates Pain Transition Through Inhibiting PKCε and TRPV1 Expression in Dorsal Root Ganglion.Frontiers in neuroscience · 2021Article
- Article
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11 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundLiver X receptors (LXRs), including LXRα and LXRβ, are key regulators of transcriptional programs for both cholesterol homeostasis and inflammation in the brain. Here, the modes of action of LXRs and the epigenetic mechanisms regulating LXRβ expression in anterior cingulate cortex (ACC) of chronic inflammatory pain (CIP) are investigated.
methodsThe deficit of LXR isoform and analgesic effect of LXR activation by GW3965 were evaluated using the mouse model of CIP induced by hindpaw injection of complete Freund's adjuvant (CFA). The mechanisms involved in GW-mediated analgesic effects were analyzed with immunohistochemical methods, ELISA, co-immunoprecipitation (Co-IP), Western blot, and electrophysiological recording. The epigenetic regulation of LXRβ expression was investigated by chromatin immunoprecipitation, quantitative real-time PCR, and sequencing.
resultsWe revealed that CFA insult led to LXRβ reduction in ACC, which was associated with upregulated expression of histone deacetylase 5 (HDAC5), and knockdown of LXRβ by shRNA led to thermal hyperalgesia. Co-IP showed that LXRβ interacted with NF-κB p65 physically. LXRβ activation by GW3965 exerted analgesic effects by inhibiting the nuclear translocation of NF-κB, reducing the phosphorylation of mitogen-activated protein kinases (MAPKs) in ACC, and decreasing the promoted input-output and enhanced mEPSC frequency in ACC neurons after CFA exposure. In vitro experiments confirmed that HDAC5 triggered histone deacetylation on the promoter region of Lxrβ, resulting in downregulation of Lxrβ transcription.
conclusionThese findings highlight an epigenetic mechanism underlying LXRβ deficits linked to CIP, and LXRβ activation may represent a potential novel target for the treatment of CIP with an alteration in inflammation responses and synaptic transmission in ACC.
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