In vitro ischemic tolerance involves upregulation of glutamate transport partly mediated by the TACE/ADAM17-tumor necrosis factor-alpha pathway

• Published in: The Journal of neuroscience Vol. 24; no. 6; pp. 1350 - 1357
• Main Authors: Romera, Cristina, Hurtado, Olivia, Botella, Sofia H, Lizasoain, Ignacio, Cárdenas, Antonio, Fernández-Tomé, Paz, Leza, Juan C, Lorenzo, Pedro, Moro, Maria A
• Format: Journal Article
• Language: English
• Published: United States Society for Neuroscience 11.02.2004
• Subjects: ADAM Proteins; ADAM17 Protein; Amino Acid Transport System X-AG - metabolism; Animals; Antibodies - pharmacology; Astrocytes - cytology; Astrocytes - metabolism; Biological Transport - physiology; Brain Ischemia - metabolism; Caspase 3; Caspases - metabolism; Cell Death - physiology; Cells, Cultured; Coculture Techniques; Enzyme Inhibitors - pharmacology; Excitatory Amino Acid Transporter 2; Excitatory Amino Acid Transporter 3; Glucose - metabolism; Glutamate Plasma Membrane Transport Proteins; Glutamic Acid - metabolism; Glutamic Acid - pharmacokinetics; Hydroxamic Acids - pharmacology; Ischemic Preconditioning; Metalloendopeptidases - antagonists & inhibitors; Metalloendopeptidases - metabolism; Neurobiology of Disease; Neurons - cytology; Neurons - drug effects; Neurons - metabolism; Rats; Rats, Wistar; Signal Transduction - physiology; Symporters - metabolism; Tumor Necrosis Factor-alpha - antagonists & inhibitors; Tumor Necrosis Factor-alpha - pharmacology; Up-Regulation

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 mod...