Linked Life Data

18774778

Source:http://linkedlifedata.com/resource/pubmed/id/18774778

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2008-10-16
pubmed:abstractText
Although reactive oxygen species have been implicated as mediators of gastrointestinal injury, their influence on the function of gastric epithelial tight junctions (TJs), which create a paracellular permeability barrier, needs to be fully investigated. H2O2 exposure to MKN28 gastric epithelial monolayers caused a significant decrease in trans-epithelial electrical resistance (TEER) and a significant increase in dextran permeability. Oxidant-mediated gastric epithelial permeability was significantly attenuated by a radical scavenger, rebamipide. H2O2 decreased the amount of claudin-3 protein but not claudin-4, -7, and JAM-A. Rebamipide significantly attenuated H2O2-induced decrease in claudin-3 protein. Small interfering RNA (siRNA) against claudin-3 treatment specifically decreased claudin-3 as seen by immunoblotting and immunofluorescent staining. Gastric TEER was significantly decreased with the treatment of siRNA against claudin-3. This is the first study to demonstrate that claudin-3 is involved in the barrier function of gastric epithelial cells and that rebamipide abolishes the H2O2-induced decrease in claudin-3 protein.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1090-2104
pubmed:author
pubmed:issnType
Electronic
pubmed:day
7
pubmed:volume
376
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
154-7
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Oxidative stress induces gastric epithelial permeability through claudin-3.
pubmed:affiliation
Division of Upper Gastroenterology, Department of Internal Medicine, Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo 663-8501, Japan.
pubmed:publicationType
Journal Article