Intraischemic mild hypothermia prevents neuronal cell death and tissue loss after neonatal cerebral hypoxia-ischemia

2006 ◽  
Vol 23 (2) ◽  
pp. 387-393 ◽  
Author(s):  
Changlian Zhu ◽  
Xiaoyang Wang ◽  
Falin Xu ◽  
Lin Qiu ◽  
Xiuyong Cheng ◽  
...  
Keyword(s):  
Cell Death ◽  
Mild Hypothermia ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Tissue Loss ◽  
Cerebral Hypoxia ◽  
Hypoxia Ischemia

Targeting Bid to prevent programmed cell death in neurons

2006 ◽  
Vol 34 (6) ◽  
pp. 1334-1340 ◽  
Author(s):  
C. Culmsee ◽  
N. Plesnila
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Neurological Diseases ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Tissue Loss ◽  
Functional Deficits ◽  
Central Nervous System Trauma ◽  
Mitochondrial Membrane Permeabilization

Sustained progression of neuronal cell death causes brain tissue loss and subsequent functional deficits following stroke or central nervous system trauma and in neurodegenerative diseases. Despite obvious differences in the pathology of these neurological disorders, the underlying delayed neuronal demise is carried out by a common biochemical cell death programme. Mitochondrial membrane permeabilization and subsequent release of apoptotic factors are key mechanisms during this process. Bcl-2 family proteins, e.g. the pro-apoptotic Bid, Bax or Bad and the antiapoptotic Bcl-2, Bcl-XL, play a crucial role in the regulation of this mitochondrial checkpoint in neurons. In particular, cleavage of cytosolic Bid and subsequent mitochondrial translocation have been detected in many paradigms of neuronal cell death related to acute or chronic neurodegeneration. The current review focuses on the emerging role of Bid as an integrating key regulator of the intrinsic death pathway that amplifies caspase-dependent and caspase-independent execution of neuronal apoptosis. Therefore pharmacological inhibition of Bid provides a promising therapeutic strategy in neurological diseases where programmed cell death is prominent.

Excitotoxic Versus Apoptotic Mechanisms of Neuronal Cell Death in Perinatal Hypoxia / Ischemia

2004 ◽  
Vol 4 (2) ◽  
pp. 77-85 ◽  
Author(s):  
Chainllie Young ◽  
Tatyana Tenkova ◽  
Krikor Dikranian ◽  
John Olney
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Perinatal Hypoxia ◽  
Hypoxia Ischemia

scholarly journals Cell Death/Proliferation and Alterations in Glial Morphology Contribute to Changes in Diffusivity in the Rat Hippocampus after Hypoxia—Ischemia

2010 ◽  
Vol 31 (3) ◽  
pp. 894-907 ◽  
Author(s):  
Miroslava Anderova ◽  
Ivan Vorisek ◽  
Helena Pivonkova ◽  
Jana Benesova ◽  
Lydia Vargova ◽  
...  
Keyword(s):  
Cell Death ◽  
Volume Fraction ◽  
Signal Transmission ◽  
Neuronal Cell Death ◽  
Three Dimensional ◽  
Neuronal Cell ◽  
Cell Number ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Hypoxia Ischemia

To understand the structural alterations that underlie early and late changes in hippocampal diffusivity after hypoxia/ischemia (H/I), the changes in apparent diffusion coefficient of water (ADCW) were studied in 8-week-old rats after H/I using diffusion-weighted magnetic resonance imaging (DW-MRI). In the hippocampal CA1 region, ADCW analyses were performed during 6 months of reperfusion and compared with alterations in cell number/cell-type composition, glial morphology, and extracellular space (ECS) diffusion parameters obtained by the real-time iontophoretic method. In the early phases of reperfusion (1 to 3 days) neuronal cell death, glial proliferation, and developing gliosis were accompanied by an ADCW decrease and tortuosity increase. Interestingly, ECS volume fraction was decreased only first day after H/I. In the late phases of reperfusion (starting 1 month after H/I), when the CA1 region consisted mainly of microglia, astrocytes, and NG2-glia with markedly altered morphology, ADCW, ECS volume fraction and tortuosity were increased. Three-dimensional confocal morphometry revealed enlarged astrocytes and shrunken NG2-glia, and in both the contribution of cell soma/processes to total cell volume was markedly increased/decreased. In summary, the ADCW increase in the CA1 region underlain by altered cellular composition and glial morphology suggests that considerable changes in extracellular signal transmission might occur in the late phases of reperfusion after H/I.

miR-21 represses FasL in microglia and protects against microglia-mediated neuronal cell death following hypoxia/ischemia

Glia ◽  
2012 ◽  
Vol 60 (12) ◽  
pp. 1888-1895 ◽  
Author(s):  
Li Zhang ◽  
Lian-Yan Dong ◽  
Ya-Jian Li ◽  
Zhen Hong ◽  
Wen-Shi Wei
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Hypoxia Ischemia

scholarly journals Neuronal cell death in neonatal hypoxia-ischemia

2011 ◽  
Vol 69 (5) ◽  
pp. 743-758 ◽  
Author(s):  
Frances J. Northington ◽  
Raul Chavez-Valdez ◽  
Lee J. Martin
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

scholarly journals Mild Hypothermia Reduces Zinc Translocation, Neuronal Cell Death, and Mortality after Transient Global Ischemia in Mice

2002 ◽  
Vol 22 (10) ◽  
pp. 1231-1238 ◽  
Author(s):  
Daisuke Tsuchiya ◽  
Shwuhuey Hong ◽  
Sang Won Suh ◽  
Takamasa Kayama ◽  
S. Scott Panter ◽  
...  
Keyword(s):  
Cell Death ◽  
Hippocampal Neurons ◽  
Mild Hypothermia ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Global Ischemia ◽  
Doppler Flowmetry ◽  
Transient Global Ischemia ◽  
Hematoxylin Eosin ◽  
Cortical Perfusion

The authors sought to determine whether Zn2+ translocation associated with neuronal cell death occurs after transient global ischemia (TGI) in mice, as has been previously shown in rats, and to determine the effect of mild hypothermia on this reaction. To validate the TGI model, carbon-black injection and laser-Doppler flowmetry were compared in three strains of mice (C57BL/6, SV129, and HSP70 transgenic mice) to assess posterior communicating artery (PcomA) development and cortical perfusion. In C57BL/6 mice, optimal results were obtained when subjected to 20-minute TGI. Brain and rectal temperature measurements were compared to monitor hypothermia. Results of TGI were compared in normothermia (NT; 37°C) and mild hypothermia groups (HT; 33°C) by staining with Zn2+-specific fluorescent dye, N-(6-methoxy-8-quinolyl)-para-toluenesulfonamide (TSQ) and hematoxylin– eosin 72 hours after reperfusion. The Zn2+ translocation observed in hippocampus CA1, CA2, and Hilus 72 hours after 20 minutes of TGI was significantly reduced by mild hypothermia. The number of degenerating neurons in the HT group was significantly less than in the NT group. Mild hypothermia reduced mortality significantly (7.1% in HT, 42.9% in NT). Results suggest that mild hypothermia may reduce presynaptic Zn2+ release in mice, which protects vulnerable hippocampal neurons from ischemic necrosis. Future studies may further elucidate mechanisms of Zn2+-induced ischemic injury.

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