Linked Life Data

11341982

Source:http://linkedlifedata.com/resource/pubmed/id/11341982

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-5-8
pubmed:abstractText
Oxygen (O(2)) species are involved in a large variety of pulmonary diseases. Among the various cell types that compose the lung, the epithelial cells of the alveolar structure appear to be a major target for oxidant injury. Despite their importance in the repair processes, the mechanisms which regulate the replication of the stem cells of the alveolar epithelium, the type 2 cells, remain poorly understood. Based on the results of several studies which have documented the involvement of the insulin-like growth factor (IGF) system in lung epithelial cell replication, and which have also suggested a role for IGF binding proteins (IGFBPs) in the control of cell proliferation, the aim of the present work was to determine whether IGFBPs could be involved in the modulation of growth of human lung epithelial cells exposed to oxidants. Experiments were performed using a human lung adenocarcinoma cell line (A549) which was exposed for various durations to hyperoxia (95% O(2)). We observed a rapid and reversible growth arrest of the cells after only 24 h of O(2) exposure. When oxidant injury was prolonged, growth arrest was followed by induction of apoptosis with activation of the Fas pathway. These effects were associated with an increased expression of IGFBP-2 and IGFBP-3. In addition, study of localization of these proteins revealed distinct patterns of distribution. IGFBP-3 was mainly present in the extracellular compartment. In comparison, the fraction of IGFBP-2 secreted was less abundant whereas the IGFBP-2 fraction in the intracellular compartment appeared stronger. In addition, analysis of the subcellular localization provided data indicating the presence of IGFBP-2 in the nucleus. Taken together these data support a role for IGFBP-2 and IGFBP-3 in the processes of growth arrest and apoptosis in lung epithelial cells upon oxidant exposure. They also suggest that distinct mechanisms may link IGFBP-2 and IGFBP-3 to the key regulators of the cell cycle.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0006-3002
pubmed:author
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
1538
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
47-58
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11341982-Acridine Orange, pubmed-meshheading:11341982-Apoptosis, pubmed-meshheading:11341982-Blotting, Western, pubmed-meshheading:11341982-Cell Division, pubmed-meshheading:11341982-Cell Nucleus, pubmed-meshheading:11341982-Epithelial Cells, pubmed-meshheading:11341982-Fluorescent Antibody Technique, pubmed-meshheading:11341982-Formaldehyde, pubmed-meshheading:11341982-Humans, pubmed-meshheading:11341982-Hyperoxia, pubmed-meshheading:11341982-Insulin-Like Growth Factor Binding Protein 2, pubmed-meshheading:11341982-Insulin-Like Growth Factor Binding Protein 3, pubmed-meshheading:11341982-Lung, pubmed-meshheading:11341982-Microscopy, Confocal, pubmed-meshheading:11341982-Oxidants, pubmed-meshheading:11341982-Polymers, pubmed-meshheading:11341982-Staining and Labeling, pubmed-meshheading:11341982-Time Factors, pubmed-meshheading:11341982-Tumor Cells, Cultured
pubmed:year
2001
pubmed:articleTitle
Distinct patterns of insulin-like growth factor binding protein (IGFBP)-2 and IGFBP-3 expression in oxidant exposed lung epithelial cells.
pubmed:affiliation
Département de Pneumologie Pédiatrique, INSERM U515, Hôpital Trousseau, Université Paris VI, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't