scholarly journals The regulatory role of NF-κB in autophagy-like cell death after focal cerebral ischemia in mice

Neuroscience ◽  
2013 ◽  
Vol 244 ◽  
pp. 16-30 ◽  
Author(s):  
W.-L. Li ◽  
S.P. Yu ◽  
D. Chen ◽  
S.S. Yu ◽  
Y.-J. Jiang ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Regulatory Role

The protective effect of lipophilic iron chelator 2, 2′-dipyridyl after focal cerebral ischemia closely correlates with limitation of apoptotic cell death

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S482-S482
Author(s):  
Michaël C Van Hoecke ◽  
Anne Prigent-Tessier ◽  
Philippe E Garnier ◽  
Christine Marie ◽  
Alain Beley
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Protective Effect ◽  
Apoptotic Cell ◽  
Focal Cerebral Ischemia ◽  
Iron Chelator ◽  
Apoptotic Cell Death

Apoptosis inducing factor (AIF) is essential for neuronal cell death following transient focal cerebral ischemia

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S466-S466
Author(s):  
Carsten Culmsee ◽  
Changlian Zhu ◽  
Miriam Höhn ◽  
Stefan Landshamer ◽  
Uta Mamrak ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Transient Focal Cerebral Ischemia ◽  
Apoptosis Inducing Factor

scholarly journals BID mediates neuronal cell death after oxygen/ glucose deprivation and focal cerebral ischemia

2001 ◽  
Vol 98 (26) ◽  
pp. 15318-15323 ◽  
Author(s):  
N. Plesnila ◽  
S. Zinkel ◽  
D. A. Le ◽  
S. Amin-Hanjani ◽  
Y. Wu ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation

Focal cerebral ischemia induces upregulation of Beclin 1 and autophagy-like cell death

2008 ◽  
Vol 29 (1) ◽  
pp. 132-141 ◽  
Author(s):  
A. Rami ◽  
A. Langhagen ◽  
S. Steiger
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Beclin 1

scholarly journals Retraction notice to “The role of ASIC1a in neuroprotection elicited by quercetin in focal cerebral ischemia” [Brain Res. Vol. 1383 (2011) 289–299]

2022 ◽  
Vol 1775 ◽  
pp. 147729
Author(s):  
Anand Kumar Pandey ◽  
Puja Panwar Hazari ◽  
Ranjana Patnaik ◽  
Anil Kumar Mishra
Keyword(s):  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Retraction Notice

scholarly journals Oxidative Stress Increases Phosphorylation of IκB Kinase-α by Enhancing NF-κB-Inducing Kinase after Transient Focal Cerebral Ischemia

2010 ◽  
Vol 30 (7) ◽  
pp. 1265-1274 ◽  
Author(s):  
Yun Seon Song ◽  
Min-Soo Kim ◽  
Hyun-Ae Kim ◽  
Bo-In Jung ◽  
Jiwon Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Nuclear Factor Κb ◽  
Nuclear Accumulation ◽  
Brain Endothelial Cells ◽  
Iκb Kinase ◽  
Transient Focal Cerebral Ischemia ◽  
Mouse Brain Endothelial Cells

The IκB kinase (IKK) complex is a central component in the classic activation of the nuclear factor-κB (NF-κB) pathway. It has been reported to function in physiologic responses, including cell death and inflammation. We have shown that IKK is regulated by oxidative status after transient focal cerebral ischemia (tFCI) in mice. However, the mechanism by which oxidative stress influences IKKs after tFCI is largely unknown. Nuclear accumulation and phosphorylation of IKKα (pIKKα) were observed 1 h after 30 mins of tFCI in mice. In copper/zinc-superoxide dismutase knockout mice, levels of NF-κB-inducing kinase (NIK) (an upstream kinase of IKKα), pIKKα, and phosphorylation of histone H3 (pH3) on Ser10 were increased after tFCI and were higher than in wild-type mice. Immunohistochemistry showed nuclear accumulation and pIKKα in mouse brain endothelial cells after tFCI. Nuclear factor-κB-inducing kinase was increased, and it enhanced pH3 by inducing pIKKα after oxygen–glucose deprivation (OGD) in mouse brain endothelial cells. Both NIK and pH3 interactions with IKKα were confirmed by coimmunoprecipitation. Treatment with IKKα small interfering RNA significantly reduced cell death after OGD. These results suggest that augmentation of NIK, IKKα, and pH3 in response to oxidative stress is involved in cell death after cerebral ischemia (or stroke).

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