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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-6-3
pubmed:abstractText
Placental 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta-HSD2) is the key enzyme which protects the fetus from overexposure to glucocorticoids (GCs) by their oxidation into inactive derivates. Several recent studies suggest that 11 beta-HSD2 expression is subjected to regulation by antenatal steroid therapy. In our study we investigated the effect of two commonly used synthetic steroids, dexamethasone (DXM) and betamethasone (BTM), on the expression and function of 11 beta-HSD2 in the rat placenta. Pregnant rats were pretreated with low (0.2mg/kg) or high (5mg/kg and 11.5mg/kg for DXM and BTM, respectively) i.m. doses of GCs. 11 beta-HSD2 expression was investigated using real-time RT-PCR and Western blotting; conversion capacity of 11 beta-HSD2 was assessed by dual perfusion of the rat placenta. Significant increase in placental 11 beta-HSD2 mRNA expression was found in rats treated with DXM, however, this alteration was not observed on protein level. BTM had no effect on either mRNA or protein levels of 11 beta-HSD2. Functional studies revealed that both GCs significantly reduced the metabolism of corticosterone by the placenta. Our data indicate that placental barrier function mediated by 11 beta-HSD2 might be considerably impaired by the antenatal therapy with DXM and BTM. In addition, the discrepancy between expressional and functional studies suggests that sole analysis of expressional changes of 11 beta-HSD2 at mRNA and/or protein levels cannot convincingly predict the role of GC treatment on 11 beta-HSD2 function in the placental barrier.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1873-1708
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
46-51
pubmed:meshHeading
pubmed-meshheading:19490994-11-beta-Hydroxysteroid Dehydrogenase Type 2, pubmed-meshheading:19490994-Animals, pubmed-meshheading:19490994-Betamethasone, pubmed-meshheading:19490994-Birth Weight, pubmed-meshheading:19490994-Blotting, Western, pubmed-meshheading:19490994-Dexamethasone, pubmed-meshheading:19490994-Dose-Response Relationship, Drug, pubmed-meshheading:19490994-Female, pubmed-meshheading:19490994-Gene Expression Regulation, pubmed-meshheading:19490994-Glucocorticoids, pubmed-meshheading:19490994-Injections, Intramuscular, pubmed-meshheading:19490994-Perfusion, pubmed-meshheading:19490994-Placenta, pubmed-meshheading:19490994-Pregnancy, pubmed-meshheading:19490994-RNA, Messenger, pubmed-meshheading:19490994-Rats, pubmed-meshheading:19490994-Rats, Wistar, pubmed-meshheading:19490994-Reverse Transcriptase Polymerase Chain Reaction
pubmed:year
2009
pubmed:articleTitle
Dexamethasone and betamethasone administration during pregnancy affects expression and function of 11 beta-hydroxysteroid dehydrogenase type 2 in the rat placenta.
pubmed:affiliation
Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Kralove, Charles University in Prague, Hradec Kralove, Czech Republic.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't