Cytoprotective Role of Prostaglandin D2 DP1 Receptor against Neuronal Injury Following Acute Excitotoxicity and Cerebral Ischemia

2015 ◽  
pp. 126-145 ◽  
Keyword(s):  
Cerebral Ischemia ◽  
Neuronal Injury ◽  
Prostaglandin D2

scholarly journals The Role of Parl and HtrA2 in Striatal Neuronal Injury After Transient Global Cerebral Ischemia

2013 ◽  
Vol 33 (11) ◽  
pp. 1658-1665 ◽  
Author(s):  
Hideyuki Yoshioka ◽  
Masataka Katsu ◽  
Hiroyuki Sakata ◽  
Nobuya Okami ◽  
Takuma Wakai ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Small Interfering Rna ◽  
Neuronal Injury ◽  
Global Cerebral Ischemia ◽  
Inhibitor Of Apoptosis ◽  
Transient Global Cerebral Ischemia ◽  
Apoptosis Protein ◽  
Interfering Rna ◽  
Ischemic Neuronal Injury

The presenilin-associated rhomboid-like (PARL) protein and high temperature requirement factor A2 (HtrA2) are key regulators of mitochondrial integrity and play pivotal roles in apoptosis. However, their roles after cerebral ischemia have not been thoroughly elucidated. To clarify these roles, mice were subjected to transient global cerebral ischemia, and striatal neuronal injury was assessed. Western blot and coimmunoprecipitation analyses revealed that PARL and processed HtrA2 localized to mitochondria, and that PARL was bound to HtrA2 in sham animals. Expression of PARL and processed HtrA2 in mitochondria significantly decreased 6 to 72 hours after ischemia, and the binding of PARL to HtrA2 disappeared after ischemia. In contrast, expression of processed HtrA2 increased 24 hours after ischemia in the cytosol, where HtrA2 was bound to X chromosome-linked inhibitor-of-apoptosis protein (XIAP). Administration of PARL small interfering RNA inhibited HtrA2 processing and worsened ischemic neuronal injury. Our results show that downregulation of PARL after ischemia is a key step in ischemic neuronal injury, and that it decreases HtrA2 processing and increases neuronal vulnerability. In addition, processed HtrA2 released into the cytosol after ischemia contributes to neuronal injury via inhibition of XIAP.

scholarly journals The Role of Polyamine Metabolism in Neuronal Injury Following Cerebral Ischemia

2009 ◽  
Vol 36 (1) ◽  
pp. 14-19 ◽  
Author(s):  
Grace H. Kim ◽  
Ricardo J. Komotar ◽  
Margy E. McCullough-Hicks ◽  
Marc L. Otten ◽  
Robert M. Starke ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Calcium Ion ◽  
Neuronal Injury ◽  
Polyamine Metabolism ◽  
Calcium Ion Channels ◽  
Secondary Damage ◽  
Reactive Aldehydes ◽  
The Us ◽  
Infarcted Tissue

Stroke is a leading cause of morbidity and mortality in the US, with secondary damage following the initial insult contributing significantly to overall poor outcome. Prior investigations have shown that the metabolism of certain polyamines such as spermine, spermidine, and putrescine are elevated in ischemic parenchyma, resulting in an increase in their metabolite concentration. Polyamine metabolites tend to be cytotoxic, leading to neuronal injury in the penumbra following stroke and expansion of the area of infarcted tissue. Although the precise mechanism is unclear, the presence of reactive aldehydes produced through polyamine metabolism, such as 3-aminopropanal and acrolein, have been shown to correlate with the incidence of cerebral vasospasm, disruption of oxidative metabolism and mitochondrial functioning, and disturbance of cellular calcium ion channels. Regulation of the polyamine metabolic pathway, therefore, may have the potential to limit injury following cerebral ischemia. To this end, we review this pathway in detail with an emphasis on clinical applicability.

Central role of neuronal IkappaBalpha kinase (IKK) in cerebral ischemia

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S458-S458
Author(s):  
Oliver Herrmann ◽  
Rossanna de Lorenzi ◽  
Sajjad Muhammad ◽  
Wen Zhang ◽  
Martin Koehrmann ◽  
...  
Keyword(s):  
Cerebral Ischemia

The Role of Melatonin in Multiple Sclerosis, Huntington's Disease and Cerebral Ischemia

2014 ◽  
Vol 13 (6) ◽  
pp. 1096-1119 ◽  
Author(s):  
Begona Escribano ◽  
Ana Colin-Gonzalez ◽  
Abel Santamaria ◽  
Isaac Tunez
Keyword(s):  
Multiple Sclerosis ◽  
Cerebral Ischemia ◽  
Huntington's Disease ◽  
Huntington’S Disease
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