Bruce/apollon promotes hippocampal neuron survival and is downregulated by kainic acidShow others and affiliations
2005 (English)In: Biochemical and Biophysical Research Communications - BBRC, ISSN 0006-291X, E-ISSN 1090-2104, Vol. 338, no 2, p. 729-735Article in journal (Refereed) Published
Abstract [en]
Prolonged or excess stimulation of excitatory amino acid receptors leads to seizures and the induction of excitotoxic nerve cell injury. Kainic acid acting on glutamate receptors produces degeneration of vulnerable neurons in parts of the hippocampus and amygdala, but the exact mechanisms are not fully understood. We have here investigated whether the anti-apoptotic protein Bruce is involved in kainic acid-induced neurodegeneration. In the rat hippocampus and cortex, Bruce was exclusively expressed by neurons. The levels of Bruce were rapidly downregulated by kainic acid in hippocampal neurons as shown both in vivo and in cell culture. Caspase-3 was activated in neurons exhibiting low levels of Bruce causing cell death. Likewise, downregulation of Bruce using antisense oligonucleotides decreased viability and enhanced the effect of kainic acid in the hippocampal neurons. The results show that Bruce is involved in neurodegeneration caused by kainic acid and the downregulation of the protein promotes neuronal death. (c) 2005 Elsevier Inc. All rights reserved.
Place, publisher, year, edition, pages
Uppsala Univ, Dept Neurosci, Neurobiol Unit, Biomed Ctr, S-75123 Uppsala, Sweden. Biomedicum Helsinki, Med Res Inst Minerva, FIN-00140 Helsinki, Finland. Univ Palermo, Dept Expt Med, Div Human Physiol, I-90134 Palermo, Italy.: ACADEMIC PRESS INC ELSEVIER SCIENCE , 2005. Vol. 338, no 2, p. 729-735
Keywords [en]
bruce/apollon, hippocampus, kainic acid, excitotoxicity, neuronal death, caspase-3, cytochrome c
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-167984DOI: 10.1016/j.bbrc.2005.09.197ISI: 000233451100007PubMedID: 16236253OAI: oai:DiVA.org:liu-167984DiVA, id: diva2:1457469
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