Delayed neuronal preconditioning with BMS-191095 is mediated by catalase

Tamas Gaspar, Anna Busija, Bela Kis, Keita Mayanagi, Christina Tulbert, James A. Snipes, F. Bari, David W. Busija

Research output: Contribution to journalArticle

Abstract

Background and aims. Selective opening of the mitochondrial ATP sensitive potassium (mitoKATP) channels with BMS-191095 (BMS) is an effective way to induce tolerance against toxic stimuli. Previous works from our laboratory demonstrated that stress-induced free radical production was completely abolished in BMS-preconditioned neurons, suggesting that improved free radical scavenging capacity plays an important role in the neuroprotective effect of BMS. The aim of our present in vitro study was to identify the mechanisms of delayed preconditioning induced by BMS. Methods. Cortical neurons of 18-day old Sprague-Dawley rat fetuses were cultured in B27 supplemented Neurobasal medium. To induce preconditioning, the neuronal cultures were treated with BMS (30 μM) once a day for 1, 2, or 3 days. Twenty-four hours after the last treatment, neuronal cultures were exposed to glutamate (200 μM) for 60 min. In some experiments, different concentrations of the catalase inhibitor 3-aminotriazole (3AT; 1, 10, 100 mM) were applied to the cultures during and for 3 hours after glutamate excitotoxicity. Cell viability was evaluated with CellTiter 96 AQueous One Solution assay on the next day. ATP levels in cortical neurons were measured using CellTiter-Glo luminescent assay. The expression of manganese dependent superoxide dismutase (MnSOD), cupper-zinc dependent superoxide dismutase (CuZnSOD), catalase, Bcl-2, and heat shock protein 70 (HsP-70) was analyzed using Western blotting. The enzymatic activity of SODs and catalase was measured with a microplate reader using commercially available kits. Results. BMS treatment resulted in higher ATP levels in resting cells (in 1E-11 mol/well: untreated, 10.65 ± 0.21; BMS 30 μM, 11.84 ± 0.22*; *p

Original languageEnglish
JournalJournal of Cerebral Blood Flow and Metabolism
Volume27
Issue numberSUPPL. 1
Publication statusPublished - Nov 13 2007

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Catalase
Neurons
Superoxide Dismutase
Free Radicals
Glutamic Acid
Adenosine Triphosphate
Amitrole
Luminescent Measurements
KATP Channels
HSP70 Heat-Shock Proteins
Poisons
Neuroprotective Agents
Sprague Dawley Rats
Zinc
Cell Survival
Fetus
Western Blotting
BMS 191095
mitochondrial K(ATP) channel
In Vitro Techniques

ASJC Scopus subject areas

  • Endocrinology
  • Neuroscience(all)
  • Endocrinology, Diabetes and Metabolism

Cite this

Gaspar, T., Busija, A., Kis, B., Mayanagi, K., Tulbert, C., Snipes, J. A., ... Busija, D. W. (2007). Delayed neuronal preconditioning with BMS-191095 is mediated by catalase. Journal of Cerebral Blood Flow and Metabolism, 27(SUPPL. 1).

Delayed neuronal preconditioning with BMS-191095 is mediated by catalase. / Gaspar, Tamas; Busija, Anna; Kis, Bela; Mayanagi, Keita; Tulbert, Christina; Snipes, James A.; Bari, F.; Busija, David W.

In: Journal of Cerebral Blood Flow and Metabolism, Vol. 27, No. SUPPL. 1, 13.11.2007.

Research output: Contribution to journalArticle

Gaspar, T, Busija, A, Kis, B, Mayanagi, K, Tulbert, C, Snipes, JA, Bari, F & Busija, DW 2007, 'Delayed neuronal preconditioning with BMS-191095 is mediated by catalase', Journal of Cerebral Blood Flow and Metabolism, vol. 27, no. SUPPL. 1.
Gaspar T, Busija A, Kis B, Mayanagi K, Tulbert C, Snipes JA et al. Delayed neuronal preconditioning with BMS-191095 is mediated by catalase. Journal of Cerebral Blood Flow and Metabolism. 2007 Nov 13;27(SUPPL. 1).
Gaspar, Tamas ; Busija, Anna ; Kis, Bela ; Mayanagi, Keita ; Tulbert, Christina ; Snipes, James A. ; Bari, F. ; Busija, David W. / Delayed neuronal preconditioning with BMS-191095 is mediated by catalase. In: Journal of Cerebral Blood Flow and Metabolism. 2007 ; Vol. 27, No. SUPPL. 1.
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AU - Tulbert, Christina

AU - Snipes, James A.

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