Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-12-25
pubmed:abstractText
The ability of cells to directly respond to glucocorticoids and aldosterone is a function of GR and MR expression, and coexpression of 11beta-hydroxysteroid dehydrogenases (11betaHSDs), which convert glucocorticoids and their 11-ketometabolites into either receptor inactive or active derivatives. The aim of the present study was to determine the cellular expression of GR, MR, 11betaHSD1, and 11betaHSD2 in neonatal rat heart and determine the role these enzymes play in modulating glucocorticoid and aldosterone action. Ribonuclease protection analysis and steroid binding assays showed that GR is expressed in both cardiac myocytes and fibroblasts, whereas MR is expressed only in myocytes. 11betaHSD2 was not detected in cardiac cells, but 11betaHSD1 was expressed at high levels in both cardiac myocytes and fibroblasts. Enzyme activity studies demonstrated that 11betaHSD1 acted as a reductase only, converting biologically inactive 11-dehydrocorticosterone to corticosterone, which then stimulated serum and glucocorticoid-induced kinase gene transcription via GR. In both cardiac myocytes and fibroblasts, aldosterone stimulated serum and glucocorticoid-induced kinase gene expression exclusively via GR, but not MR, indicating that aldosterone can have glucocorticoid-like actions in heart. The ability of cardiac cells to use both circulating corticosterone and 11-dehydrocorticosterone as a source of glucocorticoid suggests that the heart is under tonic glucocorticoid control, implying that glucocorticoids play important homeostatic roles in the heart.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/11-beta-Hydroxysteroid..., http://linkedlifedata.com/resource/pubmed/chemical/11-dehydrocorticosterone, http://linkedlifedata.com/resource/pubmed/chemical/Corticosterone, http://linkedlifedata.com/resource/pubmed/chemical/Hydroxysteroid Dehydrogenases, http://linkedlifedata.com/resource/pubmed/chemical/Immediate-Early Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Glucocorticoid, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Mineralocorticoid, http://linkedlifedata.com/resource/pubmed/chemical/serum-glucocorticoid regulated...
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
143
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
198-204
pubmed:dateRevised
2011-11-2
pubmed:meshHeading
pubmed-meshheading:11751610-11-beta-Hydroxysteroid Dehydrogenases, pubmed-meshheading:11751610-Animals, pubmed-meshheading:11751610-Animals, Newborn, pubmed-meshheading:11751610-Cells, Cultured, pubmed-meshheading:11751610-Corticosterone, pubmed-meshheading:11751610-Fibroblasts, pubmed-meshheading:11751610-Hydroxysteroid Dehydrogenases, pubmed-meshheading:11751610-Immediate-Early Proteins, pubmed-meshheading:11751610-Myocardium, pubmed-meshheading:11751610-Nuclear Proteins, pubmed-meshheading:11751610-Protein-Serine-Threonine Kinases, pubmed-meshheading:11751610-RNA, Messenger, pubmed-meshheading:11751610-Rats, pubmed-meshheading:11751610-Rats, Sprague-Dawley, pubmed-meshheading:11751610-Receptors, Glucocorticoid, pubmed-meshheading:11751610-Receptors, Mineralocorticoid, pubmed-meshheading:11751610-Transcriptional Activation
pubmed:year
2002
pubmed:articleTitle
11Beta-hydroxysteroid dehydrogenase 1 transforms 11-dehydrocorticosterone into transcriptionally active glucocorticoid in neonatal rat heart.
pubmed:affiliation
Baker Medical Research Institute, P.O. Box 6492, St. Kilda Road, Melbourne, Victoria, Australia 8008. karen.sheppard@baker.edu.au
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't