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Delayed preconditioning with BMS‐191095 increases the expression of catalase in cultured rat cortical neurons
Author(s) -
Gaspar Tamas,
Busija Anna,
Kis Bela,
Tulbert Christina,
Bari Ferenc,
Busija David
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a778-c
Subject(s) - neuroprotection , catalase , chemistry , superoxide dismutase , glutamate receptor , pharmacology , gene knockdown , in vitro , microbiology and biotechnology , biochemistry , apoptosis , enzyme , biology , receptor
Selective opening of the mitochondrial adenosine triphosphate sensitive potassium (mitoK ATP ) channels with BMS‐191095 is an effective way to induce tolerance against ischemia and other lethal stimuli. Previous works from our laboratory demonstrated that glutamate‐induced free radical production was completely abolished in BMS‐191095 preconditioned neurons, suggesting that improved free radical scavenging capacity plays an important role in the neuroprotective effect of BMS‐191095. The objective of our present in vitro study was to identify potential effectors of BMS‐191095 induced neuroprotection. Cortical neurons of 18‐day old Spraque‐Dawley rat fetuses were cultured in B27 supplemented Neurobasal medium. After 14 days in vitro the neuronal cultures were treated with BMS‐191095 (50 μM) once a day for 1, 2, or 3 days, then the cells were harvested, and protein was isolated. The expression of catalase, manganese dependent superoxide dismutase (Mn‐SOD), Bcl‐2, and heat shock protein 70 (HsP‐70) was analyzed using Western blotting. Treatment with BMS‐191095 resulted in a dose‐dependent elevation of catalase expression, whereas the protein level of Mn‐SOD, Bcl‐2, and HsP‐70 did not change. Our results indicate that catalase may play a role in the improved free radical scavenging capacity of neurons after treatment with the mitoK ATP opener BMS‐191095. Supported by NIH grants (HL‐50587, HL‐65380, HL‐77731) for D. W. Busija.