Inhibition by anandamide of 6-hydroxydopamine-induced cell death in PC12 cells.

Hdl Handle:
http://hdl.handle.net/10147/93827
Title:
Inhibition by anandamide of 6-hydroxydopamine-induced cell death in PC12 cells.
Authors:
Mnich, Katarzyna; Finn, David P; Dowd, Eilis; Gorman, Adrienne M
Affiliation:
School of Natural Sciences, National University of Ireland, Galway, Ireland.
Citation:
Inhibition by anandamide of 6-hydroxydopamine-induced cell death in PC12 cells. 2010, 2010:818497 Int J Cell Biol
Journal:
International journal of cell biology
Issue Date:
2010
URI:
http://hdl.handle.net/10147/93827
DOI:
10.1155/2010/818497
PubMed ID:
20182544
Abstract:
6-hydroxydopamine (6-OHDA) is a selective neurotoxin that is widely used to investigate cell death and protective strategies in models of Parkinson's disease. Here, we investigated the effects of the endogenous cannabinoid, anandamide, on 6-OHDA-induced toxicity in rat adrenal phaeochromocytoma PC12 cells. Morphological analysis and caspase-3 activity assay revealed that anandamide inhibited 6-OHDA-induced apoptosis. The protection was not affected by antagonists of either cannabinoid receptors (CB(1) or CB(2)) or the vanilloid receptor TRPV1. Anandamide-dependent protection was reduced by pretreatment with LY294002 (inhibitor of phosphatidylinositol 3-kinase, PI3K) and unaffected by U0126 (inhibitor of extracellularly-regulated kinase). Interestingly, phosphorylation of c-Jun-NH2-terminal kinase (JNK) in cells exposed to 6-OHDA was strongly reduced by anandamide pre-treatment. Furthermore, 6-OHDA induced c-Jun activation and increased Bim expression, both of which were inhibited by anandamide. Together, these data demonstrate antiapoptotic effects of anandamide and also suggest a role for activation of PI3K and inhibition of JNK signalling in anandamide-mediated protection against 6-OHDA.
Language:
en
ISSN:
1687-8884

Full metadata record

DC FieldValue Language
dc.contributor.authorMnich, Katarzynaen
dc.contributor.authorFinn, David Pen
dc.contributor.authorDowd, Eilisen
dc.contributor.authorGorman, Adrienne Men
dc.date.accessioned2010-03-08T13:11:52Z-
dc.date.available2010-03-08T13:11:52Z-
dc.date.issued2010-
dc.identifier.citationInhibition by anandamide of 6-hydroxydopamine-induced cell death in PC12 cells. 2010, 2010:818497 Int J Cell Biolen
dc.identifier.issn1687-8884-
dc.identifier.pmid20182544-
dc.identifier.doi10.1155/2010/818497-
dc.identifier.urihttp://hdl.handle.net/10147/93827-
dc.description.abstract6-hydroxydopamine (6-OHDA) is a selective neurotoxin that is widely used to investigate cell death and protective strategies in models of Parkinson's disease. Here, we investigated the effects of the endogenous cannabinoid, anandamide, on 6-OHDA-induced toxicity in rat adrenal phaeochromocytoma PC12 cells. Morphological analysis and caspase-3 activity assay revealed that anandamide inhibited 6-OHDA-induced apoptosis. The protection was not affected by antagonists of either cannabinoid receptors (CB(1) or CB(2)) or the vanilloid receptor TRPV1. Anandamide-dependent protection was reduced by pretreatment with LY294002 (inhibitor of phosphatidylinositol 3-kinase, PI3K) and unaffected by U0126 (inhibitor of extracellularly-regulated kinase). Interestingly, phosphorylation of c-Jun-NH2-terminal kinase (JNK) in cells exposed to 6-OHDA was strongly reduced by anandamide pre-treatment. Furthermore, 6-OHDA induced c-Jun activation and increased Bim expression, both of which were inhibited by anandamide. Together, these data demonstrate antiapoptotic effects of anandamide and also suggest a role for activation of PI3K and inhibition of JNK signalling in anandamide-mediated protection against 6-OHDA.-
dc.language.isoenen
dc.titleInhibition by anandamide of 6-hydroxydopamine-induced cell death in PC12 cells.en
dc.contributor.departmentSchool of Natural Sciences, National University of Ireland, Galway, Ireland.en
dc.identifier.journalInternational journal of cell biologyen

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