ArticleMolecular neurobiology2017
Liver X Receptor β Is Involved in Formalin-Induced Spontaneous Pain.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Inactivation of microglial LXRβ in early postnatal mice impairs microglia homeostasis and causes long-lasting cognitive dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- 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
- Spontaneous pain as a challenge of research and management in chronic pain.Medical review (2021) · 2022Review
- Sensory Neurons, Neuroimmunity, and Pain Modulation by Sex Hormones.Endocrinology · 2021Review
- Cerebral Ischemia-Reperfusion Injury: Lysophosphatidic Acid Mediates Inflammation by Decreasing the Expression of Liver X Receptor.Journal of molecular neuroscience : MN · 2020Article
- Intrathecally Administered Apelin-13 Alleviated Complete Freund's Adjuvant-Induced Inflammatory Pain in Mice.Frontiers in pharmacology · 2020Article
- Epigenetic suppression of liver X receptor β in anterior cingulate cortex by HDAC5 drives CFA-induced chronic inflammatory pain.Journal of neuroinflammation · 2019Article
- Epothilone B Benefits Nigrostriatal Pathway Recovery by Promoting Microtubule Stabilization After Intracerebral Hemorrhage.Journal of the American Heart Association · 2018Article
- Epothilone B Benefits Nigral Dopaminergic Neurons by Attenuating Microglia Activation in the 6-Hydroxydopamine Lesion Mouse Model of Parkinson's Disease.Frontiers in cellular neuroscience · 2018Article
- Propofol Exposure in Early Life Induced Developmental Impairments in the Mouse Cerebellum.Frontiers in cellular neuroscience · 2017Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence indicates that the liver X receptor(LXR) β modulates inflammatory pain. However, the molecular mechanisms through which LXRβ modulates pain are unclear. Here, we found that LXRβ-null mice responded more strongly to acute noxious stimuli than wild-type (WT) littermates (in the hot plate and Hargreaves tests) and had augmented tonic inflammatory pain (in the formalin test). This increased reactivity to inflammatory pain was accompanied by enhanced formalin-evoked Fos and pERK staining of second-order nociceptive neurons. Immunohistochemistry showed that the expression of CGRP, SP, and IB4 was increased in the lamina I-II of the lumbar dorsal horns in formalin-injected LXRβ knockout (KO) mice compared with the WT controls. In addition, LXRβ deletion in the mice enhanced the formalin-induced inflammation with more activated microglia and astrocytes in the spinal cord. Furthermore, the levels of pro-inflammatory cytokines (IL-1β ,TNF-α) as well as NFκB in the formalin-injected paw were elevated by the loss of LXRβ. Taken together, these data indicate that LXRβ is involved in acute as well as inflammatory pain, and thus, it may be considered as a new target for the development of analgesics.
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