| Anandamide protects from low serum-induced apoptosis via its degradation to ethanolamine. | |
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MedLine Citation:
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PMID: 17227767 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Anandamide (AEA) is a lipid molecule belonging to the family of endocannabinoids. Various studies report neuroprotective activity of AEA against toxic insults, such as ischemic conditions and excitotoxicity, whereas some show that AEA has pro-apoptotic effects. Here we have shown that AEA confers a protective activity in N18TG2 murine neuroblastoma cells subjected to low serum-induced apoptosis. We have demonstrated that the protection from apoptosis by AEA is not mediated via the CB1 receptor, the CB2 receptor, or the vanilloid receptor 1. Interestingly, breakdown of AEA by fatty acid amide hydrolase is required for the protective effect of AEA. Furthermore, the ethanolamine (EA) generated in this reaction is the metabolite responsible for the protective response. The elevation in the levels of reactive oxygen species during low serum-induced apoptosis is not affected by AEA or EA. On the other hand, AEA and EA reduce caspase 3/7 activity, and AEA attenuates the cleavage of PARP-1. Taken together, our results demonstrate a role for AEA and EA in the protection against low serum-induced apoptosis. |
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Authors:
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Devorah Matas; Ana Juknat; Maciej Pietr; Yael Klin; Zvi Vogel |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2007-01-16 |
Journal Detail:
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Title: The Journal of biological chemistry Volume: 282 ISSN: 0021-9258 ISO Abbreviation: J. Biol. Chem. Publication Date: 2007 Mar |
Date Detail:
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Created Date: 2007-03-12 Completed Date: 2007-04-24 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 2985121R Medline TA: J Biol Chem Country: United States |
Other Details:
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Languages: eng Pagination: 7885-92 Citation Subset: IM |
Affiliation:
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Department of Neurobiology, Weizmann Institute of Science, 76100 Rehovot, Israel. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Amidohydrolases
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metabolism Animals Apoptosis* Arachidonic Acids / pharmacology* Caspase 3 / metabolism Caspase 7 / metabolism Cell Line, Tumor DNA Fragmentation Dose-Response Relationship, Drug Ethanolamine / metabolism* Flow Cytometry Ischemia Mice Neuroblastoma / metabolism Polyunsaturated Alkamides / pharmacology* Reactive Oxygen Species Receptors, Cannabinoid / metabolism TRPV Cation Channels / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Arachidonic Acids; 0/Polyunsaturated Alkamides; 0/Reactive Oxygen Species; 0/Receptors, Cannabinoid; 0/TRPV Cation Channels; 141-43-5/Ethanolamine; 94421-68-8/anandamide; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 7; EC 3.5.-/Amidohydrolases; EC 3.5.1.-/fatty-acid amide hydrolase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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