ArticleThe Journal of pharmacology and experimental therapeutics2010
Nitro-oleic acid inhibits firing and activates TRPV1- and TRPA1-mediated inward currents in dorsal root ganglion neurons from adult male rats.
Article in The Journal of pharmacology and experimental therapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 49 citations in OpenAlex.
- The Octadecanoids: Synthesis and Bioactivity of 18-Carbon Oxygenated Fatty Acids in Mammals, Bacteria, and Fungi.Chemical reviews · 2025Review
- Dual role of transient receptor potential ankyrin 1 in respiratory and gastrointestinal physiology: From molecular mechanisms to therapeutic targets.Frontiers in physiology · 2024Review
- Systemic Lipopolysaccharide Challenge Induces Inflammatory Changes in Rat Dorsal Root Ganglia: An Ex Vivo Study.International journal of molecular sciences · 2022Article
- Nitrated Fatty-Acids Distribution in Storage Biomolecules duringAntioxidants (Basel, Switzerland) · 2022Article
- TRP Channel Agonists Activate Different Afferent Neuromodulatory Mechanisms in Guinea Pig Urinary Bladder.Frontiers in physiology · 2021Article
- Discovery of bioactive nitrated lipids and nitro-lipid-protein adducts using mass spectrometry-based approaches.Redox biology · 2019Review
- Article
- Post-Translational Modification of Proteins Mediated by Nitro-Fatty Acids in Plants: Nitroalkylation.Plants (Basel, Switzerland) · 2019Review
- The effect of the electrophilic fatty acid nitro-oleic acid on TRP channel function in sensory neurons.Nitric oxide : biology and chemistry · 2018Review
- Profile of Arachidonic Acid-Derived Inflammatory Markers and Its Modulation by Nitro-Oleic Acid in an Inherited Model of Amyotrophic Lateral Sclerosis.Frontiers in molecular neuroscience · 2018Article
- TRPA1, substance P, histamine and 5-hydroxytryptamine interact in an interdependent way to induce nociception.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Article
- TRPs in Pain Sensation.Frontiers in physiology · 2017Review
- Nitro-fatty acids in cardiovascular regulation and diseases: characteristics and molecular mechanisms.Frontiers in bioscience (Landmark edition) · 2016Review
- Generation and esterification of electrophilic fatty acid nitroalkenes in triacylglycerides.Free radical biology & medicine · 2015Article
- Inflammation-induced increase in nicotinic acetylcholine receptor current in cutaneous nociceptive DRG neurons from the adult rat.Neuroscience · 2015Article
- Activation of TRPC channels contributes to OA-NO2-induced responses in guinea-pig dorsal root ganglion neurons.The Journal of physiology · 2014Article
- Are sensory TRP channels biological alarms for lipid peroxidation?International journal of molecular sciences · 2014Review
- Sensory TRP channel interactions with endogenous lipids and their biological outcomes.Molecules (Basel, Switzerland) · 2014Review
- Nitro-oleic acid desensitizes TRPA1 and TRPV1 agonist responses in adult rat DRG neurons.Experimental neurology · 2014Article
- Redox-dependent anti-inflammatory signaling actions of unsaturated fatty acids.Annual review of physiology · 2014Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Nitro-oleic acid (OA-NO(2)), an electrophilic fatty acid by-product of nitric oxide and nitrite reactions, is present in normal and inflamed mammalian tissues at up to micromolar concentrations and exhibits anti-inflammatory signaling actions. The effects of OA-NO(2) on cultured dorsal root ganglion (DRG) neurons were examined using fura-2 Ca(2+) imaging and patch clamping. OA-NO(2) (3.5-35 microM) elicited Ca(2+) transients in 20 to 40% of DRG neurons, the majority (60-80%) of which also responded to allyl isothiocyanate (AITC; 1-50 microM), a TRPA1 agonist, and to capsaicin (CAPS; 0.5 microM), a TRPV1 agonist. The OA-NO(2)-evoked Ca(2+) transients were reduced by the TRPA1 antagonist 2-(1,3-dimethyl-2,6-dioxo-1,2,3,6-tetrahydro-7H-purin-7-yl)-N-(4-isopropylphenyl) acetamide (HC-030031; 5-50 microM) and the TRPV1 antagonist capsazepine (10 microM). Patch-clamp recording revealed that OA-NO(2) depolarized and induced inward currents in 62% of neurons. The effects of OA-NO(2) were elicited by concentrations >or=5 nM and were blocked by 10 mM dithiothreitol. Concentrations of OA-NO(2) >or=5 nM reduced action potential (AP) overshoot, increased AP duration, inhibited firing induced by depolarizing current pulses, and inhibited Na(+) currents. The effects of OA-NO(2) were not prevented or reversed by the NO-scavenger carboxy-2-phenyl-4,4,5,5-tetramethylimidazolineoxyl-1-oxyl-3-oxide. A large percentage (46-57%) of OA-NO(2)-responsive neurons also responded to CAPS (0.5 microM) or AITC (0.5 microM). OA-NO(2) currents were reduced by TRPV1 (diarylpiperazine; 5 microM) or TRPA1 (HC-030031; 5 microM) antagonists. These data reveal that endogenous OA-NO(2) generated at sites of inflammation may initially activate transient receptor potential channels on nociceptive afferent nerves, contributing to the initiation of afferent nerve activity, and later suppresses afferent firing.
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Registered trials
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