Source:http://linkedlifedata.com/resource/pubmed/id/10898727
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2000-8-17
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pubmed:abstractText |
The purpose of this study was to investigate whether the cell shrinkage that occurs during apoptosis could be explained by a change of the activity in ion transport pathways. We tested whether sphingolipids, which are potent pro-apoptotic compounds, can activate ionic currents in Xenopus laevis oocytes. Apoptosis was characterized in our model by a decrease in cell volume, a loss of cell viability, and DNA cleavage. Oocytes were studied using voltage-clamp after injection with N,N-dimethyl-D-erythrosphingosine (DMS) or D-sphingosine (DS). DMS and DS activated a fast-activating, slowly inactivating, outwardly rectifying current, similar to I(Cl-swell), a swelling-induced chloride current. Lowering the extracellular chloride dramatically reduced the current, and the channel was more selective for thiocyanate and iodide (thiocyanate > iodide) than for chloride. The current was blocked by 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB) and lanthanum but not by niflumic acid. Oocytes injected with a pseudosubstrate inhibitor of protein kinase C (PKC), PKC-(19-31), exhibited the same current. DMS-activated current was abolished by preexposure with phorbol myristate acetate. Our results suggest that induction of apoptosis in X. laevis oocytes, using sphingolipids or PKC inhibitors, activates a current similar to swelling-induced chloride current previously described in oocytes.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chloride Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/N,N-dimethylsphingosine,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Sphingolipids,
http://linkedlifedata.com/resource/pubmed/chemical/Sphingosine
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0363-6143
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
279
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
C158-65
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:10898727-Animals,
pubmed-meshheading:10898727-Apoptosis,
pubmed-meshheading:10898727-Cell Death,
pubmed-meshheading:10898727-Cells, Cultured,
pubmed-meshheading:10898727-Chloride Channels,
pubmed-meshheading:10898727-DNA Fragmentation,
pubmed-meshheading:10898727-Electric Conductivity,
pubmed-meshheading:10898727-Enzyme Inhibitors,
pubmed-meshheading:10898727-Female,
pubmed-meshheading:10898727-Oocytes,
pubmed-meshheading:10898727-Protein Kinase C,
pubmed-meshheading:10898727-Sphingolipids,
pubmed-meshheading:10898727-Sphingosine,
pubmed-meshheading:10898727-Xenopus laevis
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pubmed:year |
2000
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pubmed:articleTitle |
Induction of apoptosis using sphingolipids activates a chloride current in Xenopus laevis oocytes.
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pubmed:affiliation |
Laboratoire de Pharmacologie, Faculté de Médecine Paris Sud 94275, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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