Source:http://linkedlifedata.com/resource/pubmed/id/21356558
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rdf:type | |
lifeskim:mentions |
umls-concept:C0006675,
umls-concept:C0007765,
umls-concept:C0010453,
umls-concept:C0010837,
umls-concept:C0027882,
umls-concept:C0038435,
umls-concept:C0086045,
umls-concept:C0208973,
umls-concept:C0332157,
umls-concept:C0332453,
umls-concept:C1166758,
umls-concept:C1383501,
umls-concept:C1515926,
umls-concept:C1517892,
umls-concept:C1704666
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pubmed:issue |
3
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pubmed:dateCreated |
2011-3-14
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pubmed:abstractText |
Cytoskeleton damage is a frequent feature in neuronal cell death and one of the early events in oxidant-induced cell injury. This work addresses whether actin cytoskeleton reorganization is an early event of SIN-1-induced extracellular nitrosative/oxidative stress in cultured cerebellar granule neurons (CGN). The actin polymerization state, i.e. the relative levels of G-/F-actin, was quantitatively assessed by the ratio of the fluorescence intensities of microscopy images obtained from CGN double-labelled with Alexa594-DNase-I (for actin monomers) and Bodipy-FL-phallacidin (for actin filaments). Exposure of CGN to a flux of peroxynitrite as low as 0.5-1?M/min during 30min (achieved with 0.1mM SIN-1) was found to promote alterations of the actin cytoskeleton dynamics as it increases the G-actin/F-actin ratio. Because L-type voltage-operated Ca(2+) channels (L-VOCC) are primary targets in CGN exposed to SIN-1, the possible role of Ca(2+) dynamics on the perturbation of the actin cytoskeleton was also assessed from the cytosolic Ca(2+) concentration response to the L-VOCC's agonist FPL-64176 and to the L-VOCC's blocker nifedipine. The results showed that SIN-1 induced changes in the actin polymerization state correlated with its ability to decrease Ca(2+) influx through L-VOCC. Combined analysis of cytosolic Ca(2+) concentration and G-actin/F-actin ratio alterations by SIN-1, cytochalasin D, latrunculin B and jasplakinolide support that disruption of the actin cytoskeleton is linked to cytosolic calcium concentration changes.
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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/3-morpholino-sydnonimine,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels, L-Type,
http://linkedlifedata.com/resource/pubmed/chemical/FPL 64176,
http://linkedlifedata.com/resource/pubmed/chemical/Molsidomine,
http://linkedlifedata.com/resource/pubmed/chemical/Nifedipine,
http://linkedlifedata.com/resource/pubmed/chemical/Peroxynitrous Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrroles
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1532-1991
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pubmed:author | |
pubmed:copyrightInfo |
2011 Elsevier Ltd. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:volume |
49
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
174-83
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:21356558-Actin Cytoskeleton,
pubmed-meshheading:21356558-Animals,
pubmed-meshheading:21356558-Calcium,
pubmed-meshheading:21356558-Calcium Channel Agonists,
pubmed-meshheading:21356558-Calcium Channels, L-Type,
pubmed-meshheading:21356558-Cells, Cultured,
pubmed-meshheading:21356558-Cerebellum,
pubmed-meshheading:21356558-Molsidomine,
pubmed-meshheading:21356558-Neurons,
pubmed-meshheading:21356558-Nifedipine,
pubmed-meshheading:21356558-Oxidative Stress,
pubmed-meshheading:21356558-Peroxynitrous Acid,
pubmed-meshheading:21356558-Pyrroles,
pubmed-meshheading:21356558-Rats,
pubmed-meshheading:21356558-Rats, Wistar
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pubmed:year |
2011
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pubmed:articleTitle |
Early disruption of the actin cytoskeleton in cultured cerebellar granule neurons exposed to 3-morpholinosydnonimine-oxidative stress is linked to alterations of the cytosolic calcium concentration.
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pubmed:affiliation |
Dept. Biochemistry and Molecular Biology, Faculty of Sciences, University of Extremadura, 06006-Badajoz, Spain.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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