Linked Life Data

11738801

Source:http://linkedlifedata.com/resource/pubmed/id/11738801

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2001-12-12
pubmed:abstractText
Apoptosis contributes to uteroplacental dsyfunction in intrauterine growth retardation (IUGR). Specific protein kinase C (PKC) isoforms regulate apoptosis in other cell types. PKC isoforms thought to be anti-apoptotic include the conventional PKC isoforms (cPKC-alpha, -beta I and -beta II), whereas the novel PKC isoforms nPKC-delta and nPKC-epsilon may be apoptotic. Dexamethasone administration during the last third of pregnancy in the rat leads to IUGR. We used the dexamethasone model to test the hypothesis that adverse changes in fetal growth might be associated with a modified placental PKC isoform profile. Dexamethasone administered from day 15 of gestation via subcutaneous infusion (osmotic minipump; 100 or 200 microg dexamethasone/kg maternal body wt. per day) induced a dose-dependent decline in placental and fetal body weights at day 21 of gestation. Placental protein expression of all three cPKC isoforms was downregulated by maternal dexamethasone exposure, whereas placental nPKC-epsilon protein expression and activity was significantly upregulated in a dose-dependent manner. These data indicate that IUGR induced by excessive glucocorticoid exposure late in pregnancy leads to changes in the placental PKC isoform profile consistent with the concept that members of the PKC family participate in apoptosis signalling in the placenta.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0303-7207
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
185
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
119-26
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Possible involvement of PKC isoforms in signalling placental apoptosis in intrauterine growth retardation.
pubmed:affiliation
Department of Diabetes and Metabolic Medicine, Division of General and Developmental Medicine, St. Bartholomew's and the Royal London School of Medicine and Dentistry, Queen Mary, University of London, London E1 4NS, UK. m.c.sugden@qmw.ac.uk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't