Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
13
pubmed:dateCreated
2005-3-28
pubmed:abstractText
The NHE4 Na+/H+ exchanger is abundantly expressed on the basolateral membrane of gastric parietal cells. To test the hypothesis that it is required for normal acid secretion, NHE4-null mutant (NHE4-/-) mice were prepared by targeted disruption of the NHE4 (Slc9a4) gene. NHE4-/- mice survived and appeared outwardly normal. Analysis of stomach contents revealed that NHE4-/- mice were hypochlorhydric. The reduction in acid secretion was similar in 18-day-old, 9-week-old, and 6-month-old mice, indicating that the hypochlorhydria phenotype did not progress over time, as was observed in mice lacking the NHE2 Na+/H+ exchanger. Histological abnormalities were observed in the gastric mucosa of 9-week-old NHE4-/- mice, including sharply reduced numbers of parietal cells, a loss of mature chief cells, increased numbers of mucous and undifferentiated cells, and an increase in the number of necrotic and apoptotic cells. NHE4-/- parietal cells exhibited limited development of canalicular membranes and a virtual absence of tubulovesicles, and some of the microvilli had centrally bundled actin. We conclude that NHE4, which may normally be coupled with the AE2 Cl-/HCO3- exchanger, is important for normal levels of gastric acid secretion, gastric epithelial cell differentiation, and development of secretory canalicular and tubulovesicular membranes.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
280
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
12781-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15684419-Achlorhydria, pubmed-meshheading:15684419-Alleles, pubmed-meshheading:15684419-Alternative Splicing, pubmed-meshheading:15684419-Animals, pubmed-meshheading:15684419-Apoptosis, pubmed-meshheading:15684419-Blotting, Northern, pubmed-meshheading:15684419-Blotting, Western, pubmed-meshheading:15684419-Cell Differentiation, pubmed-meshheading:15684419-DNA, Complementary, pubmed-meshheading:15684419-Dose-Response Relationship, Drug, pubmed-meshheading:15684419-Exons, pubmed-meshheading:15684419-Gastric Acid, pubmed-meshheading:15684419-Gastrins, pubmed-meshheading:15684419-Hydrogen-Ion Concentration, pubmed-meshheading:15684419-Immunoblotting, pubmed-meshheading:15684419-In Situ Nick-End Labeling, pubmed-meshheading:15684419-Mice, pubmed-meshheading:15684419-Mice, Transgenic, pubmed-meshheading:15684419-Microscopy, Electron, pubmed-meshheading:15684419-Models, Biological, pubmed-meshheading:15684419-Models, Genetic, pubmed-meshheading:15684419-Mutation, pubmed-meshheading:15684419-Necrosis, pubmed-meshheading:15684419-Parietal Cells, Gastric, pubmed-meshheading:15684419-Phenotype, pubmed-meshheading:15684419-RNA, pubmed-meshheading:15684419-RNA, Messenger, pubmed-meshheading:15684419-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:15684419-Sodium-Hydrogen Antiporter, pubmed-meshheading:15684419-Time Factors
pubmed:year
2005
pubmed:articleTitle
Impaired gastric acid secretion in mice with a targeted disruption of the NHE4 Na+/H+ exchanger.
pubmed:affiliation
Department of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.