CIIA negatively regulates neuronal cell death induced by oxygen–glucose deprivation and reoxygenation

Sang Gil Hwang; Jaekyung Shim; Eui Ju Choi

doi:10.1007/s11010-014-2181-5

CIIA negatively regulates neuronal cell death induced by oxygen–glucose deprivation and reoxygenation

Sang Gil Hwang, Jaekyung Shim, Eui Ju Choi

Department of Life Sciences

Research output: Contribution to journal › Article › peer-review

5 Citations (Scopus)

Abstract

Brain ischemia causes neuronal injury leading to stroke and other related brain diseases. However, the precise mechanism of the ischemia-induced neuronal death remains unclear yet. In this study, we showed that CIIA suppressed neuronal cell death induced by oxygen and glucose deprivation followed by reoxygenation (OGD/R), which mimics ischemia and reperfusion in vivo, in neuroblastoma cell lines as well as primary cortical neurons. Furthermore, CIIA inhibited the OGD/R-induced stimulation of apoptosis signal-regulating kinase 1 (ASK1) and its downstream kinases including c-Jun amino-terminal kinase and p38 kinase, concomitantly blocking ASK1 homo-oligomerization and the binding between ASK1 and TRAF2. CIIA also repressed the OGD/R-induced activation of caspase-3 in neuronal cells. Taken together, our results suggest that CIIA attenuates neurotoxicity caused by OGD/R through inhibiting ASK1-dependent signaling events.

Original language	English
Pages (from-to)	139-146
Number of pages	8
Journal	Molecular and Cellular Biochemistry
Volume	397
Issue number	1-2
DOIs	https://doi.org/10.1007/s11010-014-2181-5
Publication status	Published - 2014 Oct 29

Keywords

ASK1
CIIA
Oxygen and glucose deprivation
Reoxygenation

ASJC Scopus subject areas

Molecular Biology
Clinical Biochemistry
Cell Biology

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10.1007/s11010-014-2181-5

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title = "CIIA negatively regulates neuronal cell death induced by oxygen–glucose deprivation and reoxygenation",

abstract = "Brain ischemia causes neuronal injury leading to stroke and other related brain diseases. However, the precise mechanism of the ischemia-induced neuronal death remains unclear yet. In this study, we showed that CIIA suppressed neuronal cell death induced by oxygen and glucose deprivation followed by reoxygenation (OGD/R), which mimics ischemia and reperfusion in vivo, in neuroblastoma cell lines as well as primary cortical neurons. Furthermore, CIIA inhibited the OGD/R-induced stimulation of apoptosis signal-regulating kinase 1 (ASK1) and its downstream kinases including c-Jun amino-terminal kinase and p38 kinase, concomitantly blocking ASK1 homo-oligomerization and the binding between ASK1 and TRAF2. CIIA also repressed the OGD/R-induced activation of caspase-3 in neuronal cells. Taken together, our results suggest that CIIA attenuates neurotoxicity caused by OGD/R through inhibiting ASK1-dependent signaling events.",

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author = "Hwang, {Sang Gil} and Jaekyung Shim and Choi, {Eui Ju}",

note = "Funding Information: Acknowledgments We thank Drs. H. Ichijo for ASK1 cDNA, J. Han for MKK6 cDNA. This work was supported by the National Research Foundation Grant (2006-0093855) and a NRF Grant (2011-0030141) through the National Research Foundation of Korea funded by the Ministry of Science, ICT and Future Planning (MEST) of the Korea, and by a Korea University Grant (E.-J.C.). Publisher Copyright: {\textcopyright} 2014, Springer Science+Business Media New York.",

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AU - Choi, Eui Ju

N1 - Funding Information: Acknowledgments We thank Drs. H. Ichijo for ASK1 cDNA, J. Han for MKK6 cDNA. This work was supported by the National Research Foundation Grant (2006-0093855) and a NRF Grant (2011-0030141) through the National Research Foundation of Korea funded by the Ministry of Science, ICT and Future Planning (MEST) of the Korea, and by a Korea University Grant (E.-J.C.). Publisher Copyright: © 2014, Springer Science+Business Media New York.

PY - 2014/10/29

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N2 - Brain ischemia causes neuronal injury leading to stroke and other related brain diseases. However, the precise mechanism of the ischemia-induced neuronal death remains unclear yet. In this study, we showed that CIIA suppressed neuronal cell death induced by oxygen and glucose deprivation followed by reoxygenation (OGD/R), which mimics ischemia and reperfusion in vivo, in neuroblastoma cell lines as well as primary cortical neurons. Furthermore, CIIA inhibited the OGD/R-induced stimulation of apoptosis signal-regulating kinase 1 (ASK1) and its downstream kinases including c-Jun amino-terminal kinase and p38 kinase, concomitantly blocking ASK1 homo-oligomerization and the binding between ASK1 and TRAF2. CIIA also repressed the OGD/R-induced activation of caspase-3 in neuronal cells. Taken together, our results suggest that CIIA attenuates neurotoxicity caused by OGD/R through inhibiting ASK1-dependent signaling events.

AB - Brain ischemia causes neuronal injury leading to stroke and other related brain diseases. However, the precise mechanism of the ischemia-induced neuronal death remains unclear yet. In this study, we showed that CIIA suppressed neuronal cell death induced by oxygen and glucose deprivation followed by reoxygenation (OGD/R), which mimics ischemia and reperfusion in vivo, in neuroblastoma cell lines as well as primary cortical neurons. Furthermore, CIIA inhibited the OGD/R-induced stimulation of apoptosis signal-regulating kinase 1 (ASK1) and its downstream kinases including c-Jun amino-terminal kinase and p38 kinase, concomitantly blocking ASK1 homo-oligomerization and the binding between ASK1 and TRAF2. CIIA also repressed the OGD/R-induced activation of caspase-3 in neuronal cells. Taken together, our results suggest that CIIA attenuates neurotoxicity caused by OGD/R through inhibiting ASK1-dependent signaling events.

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CIIA negatively regulates neuronal cell death induced by oxygen–glucose deprivation and reoxygenation

Abstract

Keywords

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