Role of decoy molecules in neuronal ischemic preconditioning

• Published in: Life sciences (1973) 2011-04, Vol.88 (15), p.670-674
• Main Authors: Panneerselvam, Mathivadhani, Patel, Piyush M., Roth, David M., Kidd, Michael W., Chin-Lee, Blake, Head, Brian P., Niesman, Ingrid R., Inoue, Satoki, Patel, Hemal H., Davis, Daniel P.
• Format: Article
• Language: English
• Subjects: Animals; Animals, Newborn; Apoptosis; Caffeic Acids - pharmacology; Cerebral Cortex - metabolism; death; Gene Expression Regulation; Ischemia; Ischemic Preconditioning - methods; neurons; Neurons - metabolism; NF-kappa B - antagonists & inhibitors; NF-kappa B - metabolism; Phenylethyl Alcohol - analogs & derivatives; Phenylethyl Alcohol - pharmacology; Rats; receptors; Receptors, Death Domain - metabolism; Stroke; TNF-Related Apoptosis-Inducing Ligand - metabolism; Transcription; transcription factor NF-kappa B; Tumor Necrosis Factor Decoy Receptors - metabolism; tumor necrosis factors
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/j.lfs.2011.02.004

Decoy receptors bind with TNF related apoptosis inducing ligands (TRAIL) but do not contain the cytoplasmic domains necessary to transduce apoptotic signals. We hypothesized that decoy receptors may confer neuronal protection against lethal ischemia after ischemic preconditioning (IPC). Mixed cortical neurons were exposed to IPC one day prior to TRAIL treatment or lethal ischemia. IPC increased decoy receptor but reduced death receptor expression compared to lethal ischemia. IPC-induced increase in decoy receptor expression was reduced by prior treatment with CAPE, a nuclear factor-kappa B inhibitor (NFκB). Expression of decoy molecules, dependent on NFκB, may mediate neuronal survival induced by IPC.