ArticleMolecular pain2009
Characterization of NF-kB-mediated inhibition of catechol-O-methyltransferase.
Article in Molecular pain, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- Dual CCR2/CCR5 Antagonism with Cenicriviroc Alleviates Nerve Injury-Induced Hypersensitivity and Prevents Morphine Tolerancevia Modulation of Neuroimmune Signaling.Cellular and molecular neurobiology · 2026Article
- Advances in Neuropathic Pain Research: Selected Intracellular Factors as Potential Targets for Multidirectional Analgesics.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Catechol-O-Methyltransferase Loss Drives Cell-Specific Nociceptive Signaling via the Enteric Catechol-O-Methyltransferase/microRNA-155/Tumor Necrosis Factor α Axis.Gastroenterology · 2023Article
- Catecholamines' accumulation and their disturbed metabolism at perilesional site: a possible cause of vitiligo progression.Archives of dermatological research · 2023Article
- The COMT Genetic Factor Regulates Chemotherapy-Related Prospective Memory Impairment in Survivors With HER2-/+ Breast Cancer.Frontiers in oncology · 2022Article
- The SETD6 Methyltransferase Plays an Essential Role in Hippocampus-Dependent Memory Formation.Biological psychiatry · 2020Article
- Increased cerebral nuclear factor kappa B in a complex regional pain syndrome rat model: possible relationship between peripheral injury and the brain.Journal of pain research · 2019Article
- Glucocorticoid Receptors, Brain-Derived Neurotrophic Factor, Serotonin and Dopamine Neurotransmission are Associated with Interferon-Induced Depression.The international journal of neuropsychopharmacology · 2016Article
- Targeting the Microglial Signaling Pathways: New Insights in the Modulation of Neuropathic Pain.Current medicinal chemistry · 2016Review
- Nuclear factor-kappa B regulates pain and COMT expression in a rodent model of inflammation.Brain, behavior, and immunity · 2015Article
- Actin filament reorganization in astrocyte networks is a key functional step in neuroinflammation resulting in persistent pain: novel findings on network restoration.Neurochemical research · 2015Article
- Intra-Spinal Bone Marrow Mononuclear Cells Transplantation Inhibits the Expression of Nuclear Factor-κB in Acute Transection Spinal Cord Injury in Rats.Journal of Korean Neurosurgical Society · 2014Article
- Puerarin alleviates neuropathic pain by inhibiting neuroinflammation in spinal cord.Mediators of inflammation · 2014Article
- Effect of tumour necrosis factor-alpha on estrogen metabolic pathways in breast cancer cells.Journal of Cancer · 2012Article
- Interactions between the immune and nervous systems in pain.Nature medicine · 2010Article
- Emerging role of astroglia in pain hypersensitivity.The Japanese dental science review · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCatechol-O-methyltransferase (COMT), an enzyme that metabolizes catecholamines, has recently been implicated in the modulation of pain. Specifically, low COMT activity is associated with heightened pain perception and development of musculoskeletal pain in humans as well as increased experimental pain sensitivity in rodents.
resultsWe report that the proinflammatory cytokine tumor necrosis factor alpha (TNFalpha) downregulates COMT mRNA and protein in astrocytes. Examination of the distal COMT promoter (P2-COMT) reveals a putative binding site for nuclear factor kappaB (NF-kappaB), the pivotal regulator of inflammation and the target of TNFalpha. Cell culture assays and functional deletion analyses of the cloned P2-COMT promoter demonstrate that TNFalpha inhibits P2-COMT activity in astrocytes by inducing NF-kappaB complex recruitment to the specific kappaB binding site.
conclusionCollectively, our findings provide the first evidence for NF-kappaB-mediated inhibition of COMT expression in the central nervous system, suggesting that COMT contributes to the pathogenesis of inflammatory pain states.
Indexed as
Identifiers
What OpenQuestion holds
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.