Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
25
pubmed:dateCreated
1999-7-15
pubmed:abstractText
Mouse null mutants of transcription factor ATF-2 were generated by the gene targeting method. They died shortly after birth and displayed symptoms of severe respiratory distress with lungs filled with meconium. These features are similar to those of a severe type of human meconium aspiration syndrome. The increased expression of the hypoxia inducible genes suggests that hypoxia occurs in the mutant embryos and that it may lead to strong gasping respiration with consequent aspiration of the amniotic fluid containing meconium. A reduced number of cytotrophoblast cells in the mutant placenta was found and may be responsible for an insufficient supply of oxygen prior to birth. Using the cDNA subtraction and microarray-based expression monitoring method, the expression level of the platelet-derived growth factor receptor alpha gene, which plays an important role in the proliferation of trophoblasts, was found to be low in the cytotrophoblasts of the mutant placenta. In addition, ATF-2 can trans-activate the PDGF receptor alpha gene promoter in the co-transfection assay. These results indicate the important role of ATF-2 in the formation of the placenta and the relationship between placental anomalies and neonatal respiratory distress. The ATF-2 null mutants should enhance our understanding of the mechanism of severe neonatal respiratory distress.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
18
pubmed:volume
274
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
17813-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:10364225-Activating Transcription Factor 2, pubmed-meshheading:10364225-Animals, pubmed-meshheading:10364225-Anoxia, pubmed-meshheading:10364225-Cyclic AMP Response Element-Binding Protein, pubmed-meshheading:10364225-Disease Models, Animal, pubmed-meshheading:10364225-Gene Expression Regulation, pubmed-meshheading:10364225-Gene Targeting, pubmed-meshheading:10364225-Humans, pubmed-meshheading:10364225-In Situ Hybridization, pubmed-meshheading:10364225-Infant, Newborn, pubmed-meshheading:10364225-Lung, pubmed-meshheading:10364225-Meconium Aspiration Syndrome, pubmed-meshheading:10364225-Mice, pubmed-meshheading:10364225-Mice, Knockout, pubmed-meshheading:10364225-Mutation, pubmed-meshheading:10364225-Placenta, pubmed-meshheading:10364225-Promoter Regions, Genetic, pubmed-meshheading:10364225-Receptors, Platelet-Derived Growth Factor, pubmed-meshheading:10364225-Respiratory Distress Syndrome, Newborn, pubmed-meshheading:10364225-Transcription Factors
pubmed:year
1999
pubmed:articleTitle
Mouse ATF-2 null mutants display features of a severe type of meconium aspiration syndrome.
pubmed:affiliation
Laboratory of Molecular Genetics, Tsukuba Life Science Center, RIKEN, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't