ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
In vitro ischemic tolerance involves upregulation of glutamate transport partly mediated by the TACE/ADAM17-tumor necrosis factor-alpha pathway.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 130 citations in OpenAlex.
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- Tissue-type plasminogen activator induces TNF-α-mediated preconditioning of the blood-brain barrier.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Article
- Transmembrane TNF and Its Receptors TNFR1 and TNFR2 in Mycobacterial Infections.International journal of molecular sciences · 2021Review
- Neuregulin-1 inhibits CoClMolecular brain · 2020Article
- Brain to blood efflux as a mechanism underlying the neuroprotection mediated by rapid remote preconditioning in brain ischemia.Molecular biology reports · 2020Article
- Excitatory Amino Acid Transporters in Physiology and Disorders of the Central Nervous System.International journal of molecular sciences · 2019Review
- Neuregulin1 Attenuates HNeurotoxicity research · 2019Article
- The Role of Neuronal Pentraxin 2 (NP2) in Regulating Glutamatergic Signaling and Neuropathology.Frontiers in cellular neuroscience · 2019Review
- Single Cell Immuno-Laser Microdissection Coupled to Label-Free Proteomics to Reveal the Proteotypes of Human Brain Cells After Ischemia.Molecular & cellular proteomics : MCP · 2018Article
- Sulbactam Protects Hippocampal Neurons Against Oxygen-Glucose Deprivation by Up-Regulating Astrocytic GLT-1 via p38 MAPK Signal Pathway.Frontiers in molecular neuroscience · 2018Article
- Monocyte-lymphocyte cross-communication via soluble CD163 directly links innate immune system activation and adaptive immune system suppression following ischemic stroke.Scientific reports · 2017Article
- p38 MAPK Participates in the Mediation of GLT-1 Up-regulation During the Induction of Brain Ischemic Tolerance by Cerebral Ischemic Preconditioning.Molecular neurobiology · 2017Article
- A Disintegrin and Metalloprotease 17 in the Cardiovascular and Central Nervous Systems.Frontiers in physiology · 2016Review
- Article
- Effect of Bradykinin Postconditioning on Ischemic and Toxic Brain Damage.Neurochemical research · 2015Article
- Changes in the expression of the glutamate transporter EAAT3/EAAC1 in health and disease.Cellular and molecular life sciences : CMLS · 2014Review
- Oct-2 transcription factor binding activity and expression up-regulation in rat cerebral ischaemia is associated with a diminution of neuronal damage in vitro.Neuromolecular medicine · 2014Article
- Glutamate transporters in brain ischemia: to modulate or not?Acta pharmacologica Sinica · 2014Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A short ischemic event [ischemic preconditioning (IPC)] can result in a subsequent resistance to severe ischemic injury (ischemic tolerance). Although tumor necrosis factor-alpha (TNF-alpha) contributes to the brain damage found after cerebral ischemia, its expression and neuroprotective role in models of IPC have also been described. Regarding the role of TNF-alpha convertase (TACE/ADAM17), we have recently shown its upregulation in rat brain after IPC induced by transient middle cerebral artery occlusion and that subsequent TNF-alpha release accounts for at least part of the neuroprotection found in this model. We have now used an in vitro model of IPC using rat cortical cultures exposed to sublethal oxygen-glucose deprivation (OGD) to investigate TACE expression and activity after IPC and the subsequent mechanisms of ischemic tolerance. OGD-induced cell death was significantly reduced in cells exposed to IPC by sublethal OGD 24 hr before, an effect that was inhibited by the TACE inhibitor BB3103 (1 microm) and anti-TNF-alpha antibody (2 microg/ml) and that was mimicked by TNF-alpha (10 pg/ml) preincubation. Western blot analysis showed that TACE expression is increased after IPC. IPC caused TNF-alpha release, an effect that was blocked by the selective TACE inhibitor BB-3103. In addition, IPC diminished the increase in extracellular glutamate caused by OGD and increased cellular glutamate uptake and expression of EAAT2 and EAAT3 glutamate transporters; however, only EAAT3 upregulation was mediated by increased TNF-alpha. These data demonstrate that neuroprotection induced by IPC involves upregulation of glutamate uptake partly mediated by TACE overexpression.
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