Source:http://linkedlifedata.com/resource/pubmed/id/11304499
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7
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pubmed:dateCreated |
2001-4-17
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pubmed:abstractText |
Using the whole-cell patch-clamp configuration in rat ventricular myocytes, we recently reported that microtubule disruption increases calcium current (I(Ca)) and [Ca(2+)](i) transient and accelerates their kinetics by adenylyl cyclase activation. In the present report, we further analyzed the effects of microtubule disruption by 1 micromol/L colchicine on Ca(2+) signaling in cardiac myocytes with intact sarcolemma. In quiescent intact cells, it is possible to investigate ryanodine receptor (RyR) activity by analyzing the characteristics of spontaneous Ca(2+) sparks. Colchicine treatment decreased Ca(2+) spark amplitude (F/F(0): 1.78+/-0.01, n=983, versus 1.64+/-0.01, n=1660, recorded in control versus colchicine-treated cells; P<0.0001) without modifying the sarcoplasmic reticulum Ca(2+) load and enhanced their time to peak (in ms: 6.85+/-0.09, n=1185, versus 7.33+/-0.13, n=1647; P<0.0001). Microtubule disruption also induced the appearance of Ca(2+) sparks in doublets. These alterations may reflect RyR phosphorylation. To further investigate Ca(2+) signaling in cardiac myocytes with intact sarcolemma, we analyzed [Ca(2+)](i) transient evoked by field stimulation. Cells were loaded with the fluorescence Ca(2+) indicator, Fluo-3 cell permeant, and stimulated at 1 HZ: [Ca(2+)](i) transient amplitude was greater and its decay was accelerated in colchicine-treated, field-stimulated myocytes. This effect is reversible. When colchicine-treated myocytes were placed in a colchicine-free solution for 30 minutes, tubulin was repolymerized into microtubules, as shown by immunofluorescence, and the increase in [Ca(2+)](i) transient was reversed. In summary, we demonstrate that microtubule disruption by colchicine reversibly modulates Ca(2+) signaling in cardiac cells with intact sarcolemma.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1524-4571
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
13
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pubmed:volume |
88
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
E59-65
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:11304499-Animals,
pubmed-meshheading:11304499-Calcium,
pubmed-meshheading:11304499-Calcium Signaling,
pubmed-meshheading:11304499-Cells, Cultured,
pubmed-meshheading:11304499-Colchicine,
pubmed-meshheading:11304499-Intracellular Fluid,
pubmed-meshheading:11304499-Male,
pubmed-meshheading:11304499-Microtubules,
pubmed-meshheading:11304499-Myocardium,
pubmed-meshheading:11304499-Patch-Clamp Techniques,
pubmed-meshheading:11304499-Phosphorylation,
pubmed-meshheading:11304499-Rats,
pubmed-meshheading:11304499-Rats, Wistar,
pubmed-meshheading:11304499-Recovery of Function,
pubmed-meshheading:11304499-Ryanodine Receptor Calcium Release Channel
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pubmed:year |
2001
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pubmed:articleTitle |
Microtubule disruption by colchicine reversibly enhances calcium signaling in intact rat cardiac myocytes.
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pubmed:affiliation |
Physiopathologie Cardiovasculaire, INSERM U-390, Montpellier, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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