Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2000-2-1
pubmed:abstractText
Previously, we have demonstrated that cadmium inhibits progesterone release in cultured human trophoblast cells. In the present study, we investigated potential mechanism(s) by which cadmium may elicit this effect. Cytotrophoblasts were obtained via enzymatic dispersion, purified by density gradient centrifugation, and cultured with increasing concentrations of cadmium. Cadmium-induced suppression of progesterone release seemed to be independent of cell death, as no significant decline in viability was observed with cadmium treatment. Further, immunocytochemical localization of cellular boundaries and nuclei indicated approximately 94% syncytial maturity was attained by both untreated and cadmium-treated cells, demonstrating that cadmium did not inhibit syncytial development. However, the abundance of LDL receptor (LDL-R) mRNA transcripts, as determined by competitive RT-PCR, was reduced (P < 0.05) by cadmium exposure in an apparent dose-dependent manner. Thus, the LDL-R, by which cholesterol substrate is supplied to the syncytiotrophoblast, is one site at which cadmium may interfere with placental progesterone production.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0890-6238
pubmed:author
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
473-80
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:articleTitle
Effects of cadmium cell viability, trophoblastic development, and expression of low density lipoprotein receptor transcripts in cultured human placental cells.
pubmed:affiliation
Department of Anatomy, Center for Bioenvironmental Research, Tulane University School of Medicine, New Orleans, Louisiana 70112-2699, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't