| pubmed-article:11359871 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11359871 | lifeskim:mentions | umls-concept:C0030567 | lld:lifeskim |
| pubmed-article:11359871 | lifeskim:mentions | umls-concept:C0600388 | lld:lifeskim |
| pubmed-article:11359871 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:11359871 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:11359871 | pubmed:dateCreated | 2001-5-21 | lld:pubmed |
| pubmed-article:11359871 | pubmed:abstractText | Although the toxin 6-hydroxydopamine (6-OHDA) is utilized extensively in animal models of Parkinson's disease, the underlying mechanism of its toxic effects on dopaminergic neurons is not completely understood. We examined the effects of 6-OHDA on the CNS-derived tyrosine hydroxylase expressing B65 cell line, with particular attention to the regulation of the extracellular signal-regulated protein kinases (ERK). 6-OHDA elicited a dose-dependent cytotoxicity in B65 cells. Toxic doses of 6-OHDA also elicited a biphasic pattern of ERK phosphorylation with a prominent sustained phase, a pattern that differed from that observed with hydrogen peroxide (H(2)O(2)) treatment. 6-OHDA-elicited ERK phosphorylation was blocked by PD98059, an inhibitor of the upstream mitogen activated protein kinase kinase (MEK) that phosphorylates and activates ERK. PD98059 also conferred protection against 6-OHDA cytotoxicity, but did not affect H(2)O(2) toxicity in B65 cells. These results suggest that ERK activation plays a direct mechanistic role in 6-OHDA toxicity, rather than representing a protective compensatory response, and raise the possibility that abnormal patterns of ERK activation may contribute to dopaminergic neuronal cell death. | lld:pubmed |
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| pubmed-article:11359871 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11359871 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11359871 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11359871 | pubmed:month | May | lld:pubmed |
| pubmed-article:11359871 | pubmed:issn | 0022-3042 | lld:pubmed |
| pubmed-article:11359871 | pubmed:author | pubmed-author:ChuC TCT | lld:pubmed |
| pubmed-article:11359871 | pubmed:author | pubmed-author:KulichS MSM | lld:pubmed |
| pubmed-article:11359871 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11359871 | pubmed:volume | 77 | lld:pubmed |
| pubmed-article:11359871 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11359871 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11359871 | pubmed:pagination | 1058-66 | lld:pubmed |
| pubmed-article:11359871 | pubmed:dateRevised | 2011-9-26 | lld:pubmed |
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| pubmed-article:11359871 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11359871 | pubmed:articleTitle | Sustained extracellular signal-regulated kinase activation by 6-hydroxydopamine: implications for Parkinson's disease. | lld:pubmed |
| pubmed-article:11359871 | pubmed:affiliation | Department of Pathology, Division of Neuropathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA. | lld:pubmed |
| pubmed-article:11359871 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11359871 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11359871 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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