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Plos One : Temperature Increase Exacerbates Apoptotic Neuronal Death in Chemically-induced Ischemia, Volume 8

By Vavvas, Demetrios

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Book Id: WPLBN0003967532
Format Type: PDF eBook :
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Reproduction Date: 2015

Title: Plos One : Temperature Increase Exacerbates Apoptotic Neuronal Death in Chemically-induced Ischemia, Volume 8  
Author: Vavvas, Demetrios
Volume: Volume 8
Language: English
Subject: Journals, Science, Medical Science
Collections: Periodicals: Journal and Magazine Collection (Contemporary)
Historic
Publication Date:
Publisher: Plos

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Vavvas, D. (n.d.). Plos One : Temperature Increase Exacerbates Apoptotic Neuronal Death in Chemically-induced Ischemia, Volume 8. Retrieved from http://netlibrary.net/


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Description : It is well-established that hyperthermia increases neuronal death and worsens stroke outcome. However, little is known about the mechanisms of how hyperthermia is involved in this neuronal death process. In the present study, we examined how temperature increase exacerbates neuronal death using a model of chemical ischemia. Chemical ischemia was induced by treating SH-SY5Y neuroblastoma cells with sodium azide and deoxyglucose. Temperature increase was treated by placing the cells at 37uC (control) and 41uC (experimental). Cell survival was determined by trypan blue assay and ATP levels were measured with ATP assay kits. Protein expression was detected by western blot. Treatment with sodium azide resulted in cell death in a dose-responsive manner. Increased temperature worsened the ATP depletion and cell volume shrinkage. Temperature increase also enhanced ER stress as demonstrated by the elevated level of phospho-eIF2a and C/EBP homologous protein (CHOP). Inhibition of CHOP expression significantly decreased sodium azide-induced neuronal death. In addition, the increased temperature intensified the activation of caspase-3, an apoptotic effector protease, and inhibition of capspase-3 significantly reduced cell death. These findings support that temperature increase worsened the neuronal death by depleting intracellular ATP, inducing ER stress response and activating apoptotic signal transduction.

 

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