ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
12-hydroxyeicosatetrenoate (12-HETE) attenuates AMPA receptor-mediated neurotoxicity: evidence for a G-protein-coupled HETE receptor.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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Who cites it
20 citing papers in PubMed, 48 citations in OpenAlex.
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- Fish Hydrolysate Supplementation Containing n-3 Long Chain Polyunsaturated Fatty Acids and Peptides Prevents LPS-Induced Neuroinflammation.Nutrients · 2021Article
- Exploring the molecular approach of COX and LOX in Alzheimer's and Parkinson's disorder.Molecular biology reports · 2020Review
- Qualitative and Quantitative Analysis of Regional Cerebral Free Fatty Acids in Rats Using the Stable Isotope Labeling Liquid Chromatography-Mass Spectrometry Method.Molecules (Basel, Switzerland) · 2020Article
- Mice lacking L-12/15-lipoxygenase show increased mortality during kindling despite demonstrating resistance to epileptogenesis.Epilepsia open · 2018Article
- Who is the real 12-HETrE?Prostaglandins & other lipid mediators · 2017Review
- 12-HETrE inhibits platelet reactivity and thrombosis in part through the prostacyclin receptor.Blood advances · 2017Article
- The expansive role of oxylipins on platelet biology.Journal of molecular medicine (Berlin, Germany) · 2017Review
- The Lipoxygenases: Their Regulation and Implication in Alzheimer's Disease.Neurochemical research · 2016Article
- Muscarinic inhibition of nicotinic transmission in rat sympathetic neurons and adrenal chromaffin cells.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015Article
- 12/15-Lipoxygenase metabolites of arachidonic acid activate PPARγ: a possible neuroprotective effect in ischemic brain.Journal of lipid research · 2015Article
- Temporal changes of cytochrome P450 (Cyp) and eicosanoid-related gene expression in the rat brain after traumatic brain injury.BMC genomics · 2013Article
- Emerging targets in lipid-based therapy.Biochemical pharmacology · 2013Review
- Identification of the orphan G protein-coupled receptor GPR31 as a receptor for 12-(S)-hydroxyeicosatetraenoic acid.The Journal of biological chemistry · 2011Article
- COX2 inhibitors for acquired brain injuries: is the time ripe?Critical care medicine · 2010Article
- Improved survival and reduced vascular permeability by eliminating or blocking 12/15-lipoxygenase in mouse models of acute lung injury (ALI).Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Antiinflammatory and neuroprotective actions of COX2 inhibitors in the injured brain.Brain, behavior, and immunity · 2008Review
- A liquid chromatography/mass spectrometric method for simultaneous analysis of arachidonic acid and its endogenous eicosanoid metabolites prostaglandins, dihydroxyeicosatrienoic acids, hydroxyeicosatetraenoic acids, and epoxyeicosatrienoic acids in rat brain tissue.Journal of pharmaceutical and biomedical analysis · 2007Article
- Cyclooxygenase-2-specific inhibitor improves functional outcomes, provides neuroprotection, and reduces inflammation in a rat model of traumatic brain injury.Neurosurgery · 2005Article
- Altered behavioral phenotypes in soluble epoxide hydrolase knockout mice: effects of traumatic brain injury.Prostaglandins & other lipid mediatorsArticle
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
12-hydroxyeicosatetraenoic acid (12-HETE) is a neuromodulator that is synthesized during ischemia. Its neuronal effects include attenuation of calcium influx and glutamate release as well as inhibition of AMPA receptor (AMPA-R) activation. Because 12-HETE reduces ischemic injury in the heart, we examined whether it can also reduce neuronal excitotoxicity. When treated with 12-(S)HETE, cortical neuron cultures subjected to AMPA-R-mediated glutamate toxicity suffered up to 40% less damage than untreated cultures. The protective effect of 12-(S)HETE was concentration-dependent (EC50 = 88 nm) and stereostructurally selective. Maximal protection was conferred by 300 nm 12-(S)HETE; 300 nm 15-(S)HETE was similarly protective, but 300 nm 5-(S)HETE was less effective. The chiral isomer 12-(R)HETE offered no protection; neither did arachidonic acid or 12-(S)hydroperoxyeicosatetraenoic acid. Excitotoxicity was calcium-dependent, and 12-(S)HETE was demonstrated to protect by inactivating N and L (but not P) calcium channels via a pertussis toxin-sensitive mechanism. Calcium imaging demonstrated that 12-(S)HETE also attenuates glutamate-induced calcium influx into neurons via a pertussis toxin-sensitive mechanism, suggesting that it acts via a G-protein-coupled receptor. In addition, 12-(S)HETE stimulates GTPgammaS binding (indicating G-protein activation) and inhibits adenylate cyclase in forskolin-stimulated cultures over the same concentration range as it exerts its anti-excitotoxic and calcium-influx attenuating effects. These studies demonstrate that 12-(S)HETE can protect neurons from excitotoxicity by activating a G(i/o)-protein-coupled receptor, which limits calcium influx through voltage-gated channels.
Indexed as
Identifiers
11756509PMC6757611W2120001771What 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.