Bax inhibitor-1 protects neurons from oxygen-glucose deprivation

Bax ihibitor-1 (BI-1) has been characterized as an inhibitor of Bax-induced cell death in plants and various mammalian cell systems. To explore the function of BI-1 in neurons, we overexpressed BI-1 tagged to HA or GFP in rat nigral CSM14.1 and human SH-SY5Y neuroblastoma cells. Stable BI-1 expressi...

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Bibliographic Details
Published in:	Journal of molecular neuroscience Vol. 29; no. 1; pp. 1 - 8
Main Authors:	Dohm, Christoph P, Siedenberg, Sandra, Liman, Jan, Esposito, Alessandro, Wouters, Fred S, Reed, John C, Bähr, Mathias, Kermer, Pawel
Format:	Journal Article
Language:	English
Published:	United States Springer Nature B.V 01-01-2006
Subjects:	Animals Apoptosis Apoptosis Regulatory Proteins Cell Death - drug effects Cell Line Cells Endoplasmic Reticulum - metabolism Enzyme Inhibitors - pharmacology Glucose - metabolism Humans Membrane Proteins - genetics Membrane Proteins - metabolism Neurons - cytology Neurons - drug effects Neurons - metabolism Neuroprotective Agents - metabolism Oxygen - metabolism Proteins Rats Recombinant Fusion Proteins - genetics Recombinant Fusion Proteins - metabolism Thapsigargin - pharmacology
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Summary:	Bax ihibitor-1 (BI-1) has been characterized as an inhibitor of Bax-induced cell death in plants and various mammalian cell systems. To explore the function of BI-1 in neurons, we overexpressed BI-1 tagged to HA or GFP in rat nigral CSM14.1 and human SH-SY5Y neuroblastoma cells. Stable BI-1 expression proved marked protection from cell death induced by thapsigargine, a stress agent blocking the Ca2+-ATPase of the endoplasmic reticulum (ER) but failed to inhibit cell death induced by staurosporine, a kinase inhibitor initiating mitochondria-dependent apoptosis. Moreover, BI-1 was neuroprotective in a paradigm mimicking ischemia, namely oxygen-glucose as well as serum deprivation. Examination of the subcellular distribution revealed that BI-1 predominantly locates to the ER and nuclear envelope but not mitochondria. Taken together, BI-1 overexpression in the ER is protective in neurons, making BI-1 an interesting target for future studies aiming at the inhibition of neuronal cell death during neurodegenerative diseases and stroke.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0895-8696 0895-8696 1559-1166
DOI:	10.1385/jmn:29:1:1