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Prostacyclin Mediates Endothelial Cox-2- Dependent Neuroprotective Effects During Excitotoxic Brain Injury
Author: Ying An, Natalya Belevych, Yufen Wang, Hao Zhang, Jason S Nasse, Harvey Herschman, Qun Chen, Andrew Tarr, Xiaoyu Liu, Ning Quan
Publisher: Derivative Works
11 pages
One time payment: €0.00
Required subscription: Free
Type of publication: Article
ISBN/ISSN: 1178-7031
DOI: 10.2147/JIR.S63205
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Abstract: In a previous study, we found that intracerebral administration of excitotoxin (RS)-(tetrazole-5yl) glycine caused increased neural damage in the brain in an endothelial COX-2 deleted mouse line (Tie2Cre COX-2flox/flox). In this study, we investigated whether prostacyclin might mediate this endothelial COX-2-dependent neuroprotection. Administration of excitotoxin into the striatum induced the production of prostacyclin (PGI2) in wild type, but not in endothelial COX-2 deleted mice. Inhibition of PGI2 synthase exacerbated brain lesions induced by the excitotoxin in wild type, but not in endothelial COX-2 deleted mice. Administration of a PGI2 agonist reduced neural damage in both wild type and endothelial COX-2 deleted mice. Increased PGI2 synthase expression was found in infiltrating neutrophils. In an ex vivo assay, PGI2 reduced the excitotoxin-induced calcium influx into neurons, suggesting a cellular mechanism for PGI2 mediated neuroprotection. These results reveal that PGI2 mediates endothelial COX-2 dependent neuroprotection.

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