Linked Life Data

16785550

Source:http://linkedlifedata.com/resource/pubmed/id/16785550

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-6-20
pubmed:abstractText
The role of Stat3 in the maintenance of pulmonary homeostasis following adenoviral-mediated lung injury was assessed in vivo. Stat3 was selectively deleted from bronchiolar and alveolar epithelial cells in Stat3(DeltaDelta) mice. Although lung histology and function were unaltered by deletion of Stat3 in vivo, Stat3(DeltaDelta) mice were highly susceptible to lung injury caused by intratracheal administration of AV1-GFP, an early (E) region 1- and E3-deleted, nonproliferative adenovirus. Severe airspace enlargement, loss of alveolar septae, and sloughing of the bronchiolar epithelium were observed in Stat3(DeltaDelta) mice as early as 1 day after exposure to the virus. Although surfactant protein A, B, and C content and surfactant protein-B mRNA expression in Stat3(DeltaDelta) mice were similar, TUNEL staining and caspase-3 were increased in alveolar type II epithelial cells of Stat3(DeltaDelta) mice after exposure to virus. RNA microarray analysis of type II epithelial cells isolated from Stat3(DeltaDelta) mice demonstrated significant changes in expression of numerous genes, including those genes regulating apoptosis, supporting the concept that the susceptibility of Stat3-deficient mice to adenovirus was related to the role of Stat3 in the regulation of cell survival. AV1-Bcl-x(L), an E1- and E3-deleted, nonproliferative adenovirus expressing the antiapoptotic protein Bcl-x(L), protected Stat3(DeltaDelta) mice from adenoviral-induced lung injury. Adenoviral infection of the lungs of Stat3-deficient mice was associated with severe injury of the alveolar and bronchiolar epithelium. Thus, Stat3 plays a critical cytoprotective role that is required for epithelial cell survival and maintenance of alveolar structures during the early phases of pulmonary adenoviral infection.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
177
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
527-37
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:16785550-Adenoviridae Infections, pubmed-meshheading:16785550-Animals, pubmed-meshheading:16785550-Apoptosis, pubmed-meshheading:16785550-Caspase 3, pubmed-meshheading:16785550-Caspases, pubmed-meshheading:16785550-Cell Line, pubmed-meshheading:16785550-Cytoprotection, pubmed-meshheading:16785550-Gene Expression Regulation, Viral, pubmed-meshheading:16785550-Genetic Predisposition to Disease, pubmed-meshheading:16785550-Humans, pubmed-meshheading:16785550-Intubation, Intratracheal, pubmed-meshheading:16785550-Lung, pubmed-meshheading:16785550-Mice, pubmed-meshheading:16785550-Mice, Knockout, pubmed-meshheading:16785550-Mice, Transgenic, pubmed-meshheading:16785550-Pulmonary Alveoli, pubmed-meshheading:16785550-Respiratory Mucosa, pubmed-meshheading:16785550-STAT3 Transcription Factor, pubmed-meshheading:16785550-Up-Regulation, pubmed-meshheading:16785550-bcl-X Protein
pubmed:year
2006
pubmed:articleTitle
Stat3 is required for cytoprotection of the respiratory epithelium during adenoviral infection.
pubmed:affiliation
Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural