Linked Life Data

8221125

Source:http://linkedlifedata.com/resource/pubmed/id/8221125

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1993-12-3
pubmed:abstractText
Although glucocorticoids cause growth retardation and interfere with cell development, selective promotion of some aspects of cell function also has been reported. The current study examines whether glucocorticoids enhance intracellular transduction mechanisms mediated by adenylate cyclase in the developing forebrain, a region in which steroids have been shown to interfere with cell replication, maturation, and growth. Pregnant rats were given dexamethasone at doses spanning the threshold for growth impairment (0.05, 0.2, and 0.8 mg/kg) on gestational days 17, 18, and 19, and development of adenylate cyclase was evaluated in membrane preparations, using four different activity measures; basal adenylate cyclase in the absence or presence of GTP, maximal G-protein activation by fluoride in the presence of GTP, and stimulation mediated by forskolin-Mn2+, which bypasses the G-proteins. Prenatal exposure to dexamethasone produced a dose-dependent impairment of body growth, with smaller deficits in forebrain weights (brain sparing) indicative of systemic toxicity. Basal adenylate cyclase activity was unaffected by dexamethasone treatment, regardless of whether GTP was present in the assay. Similarly, fluoride stimulation developed normally in all dexamethasone groups. However, forskolin-Mn(2+)-stimulated activity was significantly enhanced in a dose-dependent fashion. These results suggest that glucocorticoids serve as positive factors for the development of adenylate cyclase catalytic subunit activity, independently of their adverse effects on general growth and development; thus, these hormones may be a primary regulator of cell signaling during early development.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0361-9230
pubmed:author
pubmed:issnType
Print
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
359-64
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8221125-Adenylate Cyclase, pubmed-meshheading:8221125-Aging, pubmed-meshheading:8221125-Analysis of Variance, pubmed-meshheading:8221125-Animals, pubmed-meshheading:8221125-Body Weight, pubmed-meshheading:8221125-Dexamethasone, pubmed-meshheading:8221125-Female, pubmed-meshheading:8221125-Fluorides, pubmed-meshheading:8221125-Forskolin, pubmed-meshheading:8221125-GTP-Binding Proteins, pubmed-meshheading:8221125-Gestational Age, pubmed-meshheading:8221125-Guanosine Triphosphate, pubmed-meshheading:8221125-Macromolecular Substances, pubmed-meshheading:8221125-Maternal-Fetal Exchange, pubmed-meshheading:8221125-Membrane Proteins, pubmed-meshheading:8221125-Pregnancy, pubmed-meshheading:8221125-Prosencephalon, pubmed-meshheading:8221125-Rats, pubmed-meshheading:8221125-Rats, Sprague-Dawley, pubmed-meshheading:8221125-Weight Gain
pubmed:year
1993
pubmed:articleTitle
Glucocorticoids regulate the development of intracellular signaling: enhanced forebrain adenylate cyclase catalytic subunit activity after fetal dexamethasone exposure.
pubmed:affiliation
Department of Pharmacology, Duke University Medical Center, Durham, NC 27710.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.