Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2002-8-14
pubmed:abstractText
Lung liquid absorption at birth is crucial for the successful onset of respiration. Na absorption by the renal collecting duct plays an important role in renal fluid and electrolyte homeostasis during the early postnatal period. The epithelial Na channel (ENaC) plays a central role in mediating these functions, and its subunit expression is developmentally regulated in a temporal and tissue specific pattern. Several lines of evidence suggest that the prenatal increase in circulating glucocorticoids may play an important role in increasing ENaC expression during maturation. We tested the role of the prenatal surge using corticotropin-releasing hormone (CRH) knockout (KO) mice. Relative ENaC expression in lungs of KO mice increased at the same rate as in wild-type (WT) mice, but absolute expression was only 20-30% of WT. In contrast, relative and absolute expression of all three subunits in kidneys was not different between KO and WT mice. Dexamethasone (Dex) increased alpha-ENaC mRNA in fetal lung and kidney explants within 24 h but had different effects on beta- or gamma-ENaC. Dex increased beta- and gamma-ENaC in lung, but only after >48 h of exposure, and had no effect on kidney. The results suggest that the kidney metabolizes endogenous glucocorticoids, but the lung does not. Furthermore, the marked difference between lung and kidney responsiveness to glucocorticoids in beta- and gamma-ENaC expression suggests that factors other than steroids may be important in regulating functional ENaC expression during development.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0363-6143
pubmed:author
pubmed:issnType
Print
pubmed:volume
283
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
C762-72
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:12176733-Animals, pubmed-meshheading:12176733-Corticosterone, pubmed-meshheading:12176733-Corticotropin-Releasing Hormone, pubmed-meshheading:12176733-Dexamethasone, pubmed-meshheading:12176733-Epithelial Sodium Channel, pubmed-meshheading:12176733-Female, pubmed-meshheading:12176733-Gene Expression Regulation, Developmental, pubmed-meshheading:12176733-Glucocorticoids, pubmed-meshheading:12176733-Kidney, pubmed-meshheading:12176733-Lung, pubmed-meshheading:12176733-Maternal-Fetal Exchange, pubmed-meshheading:12176733-Mice, pubmed-meshheading:12176733-Mice, Knockout, pubmed-meshheading:12176733-Nuclease Protection Assays, pubmed-meshheading:12176733-Phenotype, pubmed-meshheading:12176733-Pregnancy, pubmed-meshheading:12176733-RNA, Messenger, pubmed-meshheading:12176733-Sodium Channels
pubmed:year
2002
pubmed:articleTitle
Endogenous and exogenous glucocorticoid regulation of ENaC mRNA expression in developing kidney and lung.
pubmed:affiliation
Department of Internal Medicine, University of Iowa College of Medicine and Veterans Affairs Medical Center, Iowa City 52242, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't