Global Brain Ischemia and Reperfusion: Modifications in Eukaryotic Initiation Factors Associated with Inhibition of Translation Initiation

2002 ◽  
Vol 67 (5) ◽  
pp. 2005-2012 ◽  
Author(s):  
Donald J. DeGracia ◽  
Robert W. Neumar ◽  
Blaine C. White ◽  
Gary S. Krause
Keyword(s):  
Brain Ischemia ◽  
Translation Initiation ◽  
Ischemia And Reperfusion ◽  
Global Brain Ischemia ◽  
Factors Associated ◽  
Initiation Factors ◽  
Eukaryotic Initiation Factors ◽  
Global Brain

scholarly journals HuR Function and Translational State Analysis Following Global Brain Ischemia and Reperfusion

2013 ◽  
Vol 4 (6) ◽  
pp. 589-603 ◽  
Author(s):  
Jeffrey J. Szymanski ◽  
Haihui Wang ◽  
Jill T. Jamison ◽  
Donald J. DeGracia
Keyword(s):  
Brain Ischemia ◽  
Ischemia And Reperfusion ◽  
Global Brain Ischemia ◽  
Global Brain ◽  
State Analysis

scholarly journals Calpain Mediates Eukaryotic Initiation Factor 4G Degradation during Global Brain Ischemia

1998 ◽  
Vol 18 (8) ◽  
pp. 876-881 ◽  
Author(s):  
Robert W. Neumar ◽  
Donald J. DeGracia ◽  
Lynette L. Konkoly ◽  
John I. Khoury ◽  
Blaine C. White ◽  
...  
Keyword(s):  
Brain Ischemia ◽  
Critical Role ◽  
Initiation Factor ◽  
Ischemia And Reperfusion ◽  
Eukaryotic Initiation Factor ◽  
Global Brain Ischemia ◽  
Eukaryotic Initiation Factor 4G ◽  
Global Brain ◽  
Calpain Inhibitors

Global brain ischemia and reperfusion result in the degradation of the eukaryotic initiation factor (eIF) 4G, which plays a critical role in the attachment of the mRNA to the ribosome. Because eIF-4G is a substrate of calpain, these studies were undertaken to examine whether calpain I activation during global brain ischemia contributes to the degradation of eIF-4G in vivo. Immunoblots with antibodies against calpain I and eIF-4G were prepared from rat brain postmitochondrial supernatant incubated at 37°C with and without the addition of calcium and the calpain inhibitors calpastatin or MDL-28,170. Addition of calcium alone resulted in calpain I activation (as measured by autolysis of the 80-kDa subunit) and degradation of eIF-4G; this effect was blocked by either 1 μmol/L calpastatin or 10 μmol/L MDL-28,170. In rabbits subjected to 20 minutes of cardiac arrest, immunoblots of brain postmitochondrial supernatants showed that the percentage of autolyzed calpain I increased from 1.9% ± 1.1% to 15.8% ± 5.0% and that this was accompanied by a 68% loss of eIF-4G. MDL-28,170 pretreatment (30 mg/kg) decreased ischemia-induced calpain I autolysis 40% and almost completely blocked eIF-4G degradation. We conclude that calpain I degrades eIF-4G during global brain ischemia.

Hippocampal Cellular Stress Responses After Global Brain Ischemia and Reperfusion

2007 ◽  
Vol 9 (12) ◽  
pp. 2265-2276 ◽  
Author(s):  
George G. Roberts ◽  
Mike J. Di Loreto ◽  
Monique Marshall ◽  
Jie Wang ◽  
Donald J. DeGracia
Keyword(s):  
Brain Ischemia ◽  
Stress Responses ◽  
Cellular Stress ◽  
Ischemia And Reperfusion ◽  
Global Brain Ischemia ◽  
Cellular Stress Responses ◽  
Global Brain

scholarly journals The effects of Y-27632 on pial microvessels during global brain ischemia and reperfusion in rabbits

2017 ◽  
Vol 17 (1) ◽  
Author(s):  
Noriyuki Shintani ◽  
Tadahiko Ishiyama ◽  
Masakazu Kotoda ◽  
Nobumasa Asano ◽  
Daniel I. Sessler ◽  
...  
Keyword(s):  
Brain Ischemia ◽  
Ischemia And Reperfusion ◽  
Global Brain Ischemia ◽  
Pial Microvessels ◽  
Global Brain

Global brain ischemia and reperfusion: Golgi apparatus ultrastructure in neurons selectively vulnerable to death

1995 ◽  
Vol 90 (1) ◽  
pp. 17-30 ◽  
Author(s):  
Jos� A. Rafols ◽  
Asif M. Daya ◽  
Brian J. O'Neil ◽  
Gary S. Krause ◽  
Robert W. Neumar ◽  
...  
Keyword(s):  
Golgi Apparatus ◽  
Brain Ischemia ◽  
Ischemia And Reperfusion ◽  
Global Brain Ischemia ◽  
Global Brain

Global brain ischemia and reperfusion

2010 ◽  
pp. 236-281 ◽  
Author(s):  
Brian J. O'Neil ◽  
Raymond C. Koehler ◽  
Robert W. Neumar ◽  
Uwe Ebmeyer ◽  
Gary S. Krause
Keyword(s):  
Brain Ischemia ◽  
Ischemia And Reperfusion ◽  
Global Brain Ischemia ◽  
Global Brain
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