Linked Life Data

11589620

Source:http://linkedlifedata.com/resource/pubmed/id/11589620

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2001-10-8
pubmed:abstractText
We have studied the effect of enhanced expression of epithelial Na(+)channels (ENaC) on the ATP-induced Cl(-)secretion in the mouse epithelium using short-circuit current (I(SC)) and RT-PCR techniques. The amiloride sensitivity of basal current (I(b)) across the cultured endometrial epithelia was found to vary with the magnitude of the I(b), the higher the I(b)the greater its sensitivity to amiloride, indicating possible elevation of ENaC. However, the magnitude of ATP-induced I(SC), previously demonstrated to be mediated by Ca(2+)-activated chloride channel (CaCC), decreased as the amiloride sensitivity of the I(b)increased, suggesting a possible inhibitory effect of elevated expression of ENaC on ATP-mediated chloride secretion. The Matrigel treatment for culturing the endometrial epithelia affected the amiloride sensitivity of the I(b)as well as the ATP-induced I(SC)reversedly. Competitive RT-PCR demonstrated that the expression of both ENaC gamma subunits and CaCC was enhanced in Matrigel-treated cultures. However, the observed reduction in the ATP-induced or CaCC-mediated I(SC)could not be explained by the CaCC expression pattern. These data suggest that inhibition of CaCC function is due to enhanced ENaC expression. Therefore, in addition to interacting with CFTR, ENaC also appears to interact with CaCC in the mouse endometrial epithelium. Physiologically the present findings indicate that enhanced expression of ENaC leads to suppression of other Cl(-)channels, such as CFTR and CaCC, thereby preconditioning the endometrium in favour of overall salt and water absorption as observed during embryo implantation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1065-6995
pubmed:author
pubmed:copyrightInfo
Copyright 2001 Academic Press.
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1017-20
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Suppression of ATP-induced Cl(-)secretion by enhanced expression of epithelial Na(+)channels in mouse endometrial epithelium.
pubmed:affiliation
Epithelial Cell Biology Research Center, Department of Physiology, Faculty of Medicine, Chinese University of Hong Kong, Shatin, Hong Kong.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't