Linked Life Data

16885151

Source:http://linkedlifedata.com/resource/pubmed/id/16885151

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-1-9
pubmed:abstractText
Under hypoxia, some cells survive and others are irreversibly injured and die. The factors that determine cell fate under stress remain largely unknown. We recently selected death-resistant cells via repeated episodes of hypoxia. In the present study, 80 clones were isolated from the selected cells and their response to apoptotic injury was characterized. Compared with the wild-type cells, the isolated clones showed a general resistance to apoptosis: 13 were extremely resistant to azide-induced apoptosis, 10 to staurosporine, and 9 to cisplatin. The cell clones that most consistently demonstrated resistance or sensitivity to injury were further studied for their response to azide treatment. Azide induced comparable ATP depletion in these clones and wild-type cells. Hypoxia inducible factor-1 (HIF-1) was upregulated in several clones, but the upregulation did not correlate with cell death resistance. The selected clones maintained an epithelial phenotype, showing typical epithelial morphology, forming "domes" at high density, and expressing E-cadherin. Azide-induced Bax translocation and cytochrome c release, two critical mitochondrial events of apoptosis, were abrogated in death-resistant clones. In addition, cell lysates isolated from these clones showed lower caspase activation on addition of exogenous cytochrome c. Bax, Bak, and Bid expression in these clones was similar to that in wild-type cells, whereas Bcl-2 expression was higher in all the selected clones and, interestingly, Bcl-xL was markedly upregulated in the most death-resistant clones. The results suggest that apoptotic resistance of the selected clones is not determined by a single factor or molecule but, rather, by various alterations at the core apoptotic pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1931-857X
pubmed:author
pubmed:issnType
Print
pubmed:volume
292
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
F243-52
pubmed:dateRevised
2011-4-28
pubmed:meshHeading
pubmed-meshheading:16885151-Adenosine Triphosphate, pubmed-meshheading:16885151-Animals, pubmed-meshheading:16885151-Apoptosis, pubmed-meshheading:16885151-Azides, pubmed-meshheading:16885151-Cadherins, pubmed-meshheading:16885151-Caspases, pubmed-meshheading:16885151-Cell Hypoxia, pubmed-meshheading:16885151-Cisplatin, pubmed-meshheading:16885151-Clone Cells, pubmed-meshheading:16885151-Cytochromes c, pubmed-meshheading:16885151-Enzyme Activation, pubmed-meshheading:16885151-Epithelial Cells, pubmed-meshheading:16885151-Fluorescent Antibody Technique, pubmed-meshheading:16885151-Hypoxia-Inducible Factor 1, alpha Subunit, pubmed-meshheading:16885151-Immunoblotting, pubmed-meshheading:16885151-Kidney Tubules, Proximal, pubmed-meshheading:16885151-Phenotype, pubmed-meshheading:16885151-Protein Transport, pubmed-meshheading:16885151-Rats, pubmed-meshheading:16885151-Staurosporine, pubmed-meshheading:16885151-Subcellular Fractions, pubmed-meshheading:16885151-bcl-2-Associated X Protein, pubmed-meshheading:16885151-bcl-X Protein
pubmed:year
2007
pubmed:articleTitle
Characterization of cell clones isolated from hypoxia-selected renal proximal tubular cells.
pubmed:affiliation
Department of Cellular Biology and Anatomy, Medical College of Georgia, and Veterans Affairs Medical Center, Augusta, Georgia 30912, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, N.I.H., Extramural