Linked Life Data

9737950

Source:http://linkedlifedata.com/resource/pubmed/id/9737950

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1998-10-26
pubmed:abstractText
The effects of cytochalasin D, a specific F-actin depolymerizing agent, on Ca2+ transients in rat ventricular cardiomyocytes were investigated. Cytochalasin D (20 microM) significantly slowed decay of Ca2+ transients (tau decay control cells=28.1+/-1.3, n=28tau decay=47.3+/-2.8 ms, n=20, P<0.001). The rising phase of Ca2+ transients was also significantly slower in cytochalasin D treated cells (tau rise=5.1+/-0.6 ms, n=17nu tau rise in control cells=3.6+/-0.2, n=21,P<0.01). Phalloidin (100 microM), an F-actin stabilizer, prevented cytochalasin D-induced alterations of Ca2+ transient kinetics. The cytochalasin D effect was not related to the l-type Ca2+ current since the current density and kinetics were not altered by the drug. We conclude that integrity of F-actin-based cytoskeleton is an important factor for sarcoplasmic reticulum function.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-2828
pubmed:author
pubmed:copyrightInfo
Copyright 1998 Academic Press.
pubmed:issnType
Print
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1665-70
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Cytochalasin D alters kinetics of Ca2+ transient in rat ventricular cardiomyocytes: an effect of altered actin cytoskeleton?
pubmed:affiliation
Department of Cardiovascular Medicine, Henry Ford Heart and Vascular Institute, 2799 West Grand Boulevard, Detroit, MI, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.