Linked Life Data

12208465

Source:http://linkedlifedata.com/resource/pubmed/id/12208465

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2002-9-4
pubmed:abstractText
We investigated the role of intracellular calcium ([Ca(2+)](i)) in adhesion molecule expression in human umbilical vascular endothelial cells (HUVECs). Calmodulin (CaM) antagonists, W-7, trifluoperazine and chlorpromazine, triggered a rise in [Ca(2+)](i) in HUVECs. In the presence of extracellular Ca(2+), thapsigargin pretreatment completely prevented W-7-stimulated increase in [Ca(2+)](i), indicating that increase is attributable to the release of Ca(2+) from internal stores. The increased [Ca(2+)](i) acted as a second messenger to enhance tumor necrosis factor-alpha (TNF-alpha)-induced E-selectin and suppress intercellular cell adhesion molecule (ICAM-1) expression. Preincubation of HUVECs with the Ca(2+) chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraaceticacetomethyl ester blocked W-7-mediated effects on E-selectin and ICAM-1. The W-7 effects were paralleled by changes in the respective mRNAs, suggesting regulation at a pretranslational level. These findings indicate that CaM-regulated [Ca(2+)](i) in HUVECs may play an important role in controlling expression of endothelial adhesion molecules involved in atherogenesis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0021-9150
pubmed:author
pubmed:issnType
Print
pubmed:volume
165
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5-13
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Increased intracellular calcium transients by calmodulin antagonists differentially modulate tumor necrosis factor-alpha-induced E-selectin and ICAM-1 expression.
pubmed:affiliation
Department of Medicine, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA. kchen@niaid.nih.gov
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't