Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
32
pubmed:dateCreated
1997-9-5
pubmed:abstractText
This report examines the effect of cell volume expansion on cyclooxygenase-2 (COX-2) mRNA expression, COX-2 protein expression, and prostaglandin E2 release from human amnion-derived WISH cells. Earle's balanced salts solution (EBSS) with limited NaCl concentration was utilized as the induction medium. COX-2 mRNA was elevated 6-fold in cells incubated for 1 h in hypotonic EBSS. COX-2 mRNA expression was not increased when raffinose or sucrose were used to reconstitute low NaCl. Actinomycin D blocked COX-2 mRNA increase by hypotonic stress, while cycloheximide enhanced COX-2 mRNA expression. COX-2 mRNA and protein concentrations increased as a function of decreasing media osmolarity and incubation time in hypotonic EBSS. Hypotonic EBSS induced a 3-fold increase in prostaglandin E2 release. WISH cells transiently transfected with a luciferase expression vector driven by the human COX-2 promoter for the COX-2 gene show a 3-fold increase in luciferase activity when incubated in hypotonic EBSS. COX-2 mRNA levels in primary human amnion cells were also increased by hypotonic stress. This study suggests that amnion cell COX-2 gene expression is regulated by cell volume expansion and/or increased plasma membrane tension.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
8
pubmed:volume
272
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
20118-24
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Hypotonic stress increases cyclooxygenase-2 expression and prostaglandin release from amnion-derived WISH cells.
pubmed:affiliation
Labor Focus Research Group, Case Western Reserve University School of Medicine, MetroHealth Medical Center, Cleveland, Ohio 44109, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't