Linked Life Data

11140697

Source:http://linkedlifedata.com/resource/pubmed/id/11140697

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2001-1-3
pubmed:abstractText
Exposure of the lung to severe hyperoxia induces terminal transferase dUTP end-labeling (TUNEL) indicative of DNA damage or apoptosis and increases expression of the tumor suppressor p53 and of members of the Bcl-2 gene family. Because cell survival and apoptosis are regulated, in part, by the relative abundance of proteins of the Bcl-2 family, we hypothesized that lung cells dying during exposure would show increased expression of pro-apoptotic members, such as Bax, whereas surviving cells would have increased expression of anti-apoptotic members, such as Bcl-X(L). The hypothesis is tested in the current study by determining which Bcl-2 genes are regulated by hyperoxia, with specific focus on correlating expression of Bax and Bcl-X(L) with morphologic evidence of apoptosis or necrosis. Adult mice exposed to greater than 95% oxygen concentrations for 48 to 88 hours had increased whole-lung mRNA levels of Bax and Bcl-X(L), no change in Bak, Bad, or Bcl-2, and decreased levels of Bcl-w and Bfl-1. In situ hybridization revealed that hyperoxia induced Bax and Bcl-X(L) mRNA in uniform and overlapping patterns of expression throughout terminal bronchioles and parenchyma, coinciding with TUNEL staining. Electron microscopy and DNA electrophoresis, however, suggested relatively little classical apoptosis. Unexpectedly, Western analysis demonstrated increased Bcl-X(L), but not Bax, protein in response to hyperoxia. Bax and Bfl-1 were not altered by hyperoxia in p53 null mice; however, oxygen toxicity was not lessened by p53 deficiency. These findings suggest that oxygen-induced lung injury does not depend on the relative expression of these Bcl-2 members.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0023-6837
pubmed:author
pubmed:issnType
Print
pubmed:volume
80
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1845-54
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11140697-Animals, pubmed-meshheading:11140697-Apoptosis, pubmed-meshheading:11140697-Cell Survival, pubmed-meshheading:11140697-DNA Damage, pubmed-meshheading:11140697-Gene Expression Regulation, pubmed-meshheading:11140697-Genes, bcl-2, pubmed-meshheading:11140697-Genes, p53, pubmed-meshheading:11140697-Hyperoxia, pubmed-meshheading:11140697-In Situ Nick-End Labeling, pubmed-meshheading:11140697-Lung, pubmed-meshheading:11140697-Lung Diseases, pubmed-meshheading:11140697-Male, pubmed-meshheading:11140697-Mice, pubmed-meshheading:11140697-Mice, Inbred C57BL, pubmed-meshheading:11140697-Mice, Knockout, pubmed-meshheading:11140697-Proteins, pubmed-meshheading:11140697-Proto-Oncogene Proteins, pubmed-meshheading:11140697-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:11140697-RNA, Messenger, pubmed-meshheading:11140697-Transcription, Genetic, pubmed-meshheading:11140697-bcl-2-Associated X Protein, pubmed-meshheading:11140697-bcl-X Protein
pubmed:year
2000
pubmed:articleTitle
Bcl-2 family gene expression during severe hyperoxia induced lung injury.
pubmed:affiliation
Department of Pediatrics, School of Medicine and Dentistry, Children's Hospital at Strong, University of Rochester, New York 14642, USA. michael_oreilly@urmc.rochester.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't