Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-3-17
pubmed:abstractText
Endothelin-1 (ET-1) is released in various cardiovascular disorders including congestive heart failure, and may modulate significantly the disease process by its potent action on vascular and cardiac muscle cell function and gene regulation. In adult mouse ventricular cardiomyocytes loaded with indo-1, ET-1 induced a sustained negative inotropic effect (NIE) in association with decreases in Ca(2+) transients. The ET-1-induced effects on Ca(2+) transients and cell shortening were abolished in diacylglycerol (DAG) kinase zeta-overexpressing mouse ventricular myocytes. A nonselective protein kinase C (PKC) inhibitor, GF109203X, inhibited the ET-1-induced decreases in Ca(2+) transients and cell shortening in concentration-dependent manners, whereas a selective Ca(2+)-dependent PKC inhibitor, Gö6976, did not affect the ET-1-induced effects. A phospholipase Cbeta inhibitor, U73122, and an inhibitor of phospholipase D, C(2)-ceramide, partially, but significantly, attenuated the ET-1-induced effects. Derivatives of the respective inhibitors with no specific effects, U73343 and dihydro-C(2)-ceramide, did not affect the ET-1-induced effects. Taken together, these results indicate that activation of a Ca(2+)-independent PKC isozyme by 1,2-DAG, which is generated by phospholipase Cbeta and phospholipase D activation and inactivated by phosphorylation via DAG kinase, is responsible for the ET-1-induced decreases in Ca(2+) transients and cell shortening in mouse ventricular cardiomyocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1095-8584
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
44
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
520-6
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Overexpression of diacylglycerol kinase zeta inhibits endothelin-1-induced decreases in Ca2+ transients and cell shortening in mouse ventricular myocytes.
pubmed:affiliation
Department of Cardiovascular Pharmacology, Yamagata University School of Medicine, 2-2-2 Iida-nishi, Yamagata, 990-9585 Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't