Source:http://linkedlifedata.com/resource/pubmed/id/18981098
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
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pubmed:dateCreated |
2008-11-4
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pubmed:abstractText |
Ca(2+)-mediated signal transduction pathways play a central regulatory role in dendritic cell (DC) responses to diverse Ags. However, the mechanisms leading to increased [Ca(2+)](i) upon DC activation remained ill-defined. In the present study, LPS treatment (100 ng/ml) of mouse DCs resulted in a rapid increase in [Ca(2+)](i), which was due to Ca(2+) release from intracellular stores and influx of extracellular Ca(2+) across the cell membrane. In whole-cell voltage-clamp experiments, LPS-induced currents exhibited properties similar to the currents through the Ca(2+) release-activated Ca(2+) channels (CRAC). These currents were highly selective for Ca(2+), exhibited a prominent inward rectification of the current-voltage relationship, and showed an anomalous mole fraction and a fast Ca(2+)-dependent inactivation. In addition, the LPS-induced increase of [Ca(2+)](i) was sensitive to margatoxin and ICAGEN-4, both inhibitors of voltage-gated K(+) (Kv) channels Kv1.3 and Kv1.5, respectively. MHC class II expression, CCL21-dependent migration, and TNF-alpha and IL-6 production decreased, whereas phagocytic capacity increased in LPS-stimulated DCs in the presence of both Kv channel inhibitors as well as the I(CRAC) inhibitor SKF-96365. Taken together, our results demonstrate that Ca(2+) influx in LPS-stimulated DCs occurs via Ca(2+) release-activated Ca(2+) channels, is sensitive to Kv channel activity, and is in turn critically important for DC maturation and functions.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels, Voltage-Gated,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1550-6606
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
15
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pubmed:volume |
181
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6803-9
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pubmed:meshHeading |
pubmed-meshheading:18981098-Animals,
pubmed-meshheading:18981098-Calcium Channels,
pubmed-meshheading:18981098-Cell Differentiation,
pubmed-meshheading:18981098-Cell Movement,
pubmed-meshheading:18981098-Dendritic Cells,
pubmed-meshheading:18981098-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:18981098-Female,
pubmed-meshheading:18981098-Flow Cytometry,
pubmed-meshheading:18981098-Immunohistochemistry,
pubmed-meshheading:18981098-Interleukin-6,
pubmed-meshheading:18981098-Lipopolysaccharides,
pubmed-meshheading:18981098-Membrane Potentials,
pubmed-meshheading:18981098-Mice,
pubmed-meshheading:18981098-Patch-Clamp Techniques,
pubmed-meshheading:18981098-Potassium Channels, Voltage-Gated,
pubmed-meshheading:18981098-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:18981098-Tumor Necrosis Factor-alpha
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pubmed:year |
2008
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pubmed:articleTitle |
Ion channels modulating mouse dendritic cell functions.
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pubmed:affiliation |
Department of Physiology, University of Tübingen, Gmelinstr. 5, Tübingen, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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