Linked Life Data

8635489

Source:http://linkedlifedata.com/resource/pubmed/id/8635489

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1996-7-8
pubmed:abstractText
Heat shock treatment of cells increases their survival and resistance to apoptosis. The kinetics of development of this resistance correlates with the kinetics of synthesis of heat shock proteins (hsps). U937 and Wehi-s cells were cultured for 1 h at 42 degrees C, conditions which induced the synthesis of heat shock proteins 27, 70, and 90. The cells were subsequently permitted to recover for a 2-h period, prior to exposure to the apoptosis inducing agents actinomycin-D (5 micrograms/ml), camptothecin (5 micrograms/ml), and etoposide (25 micrograms/ml). Apoptosis was determined by both DNA fragmentation and flow cytometric analysis. Heat-shocked cultures had a smaller number of apoptotic compared to control cultures when both were exposed to apoptosis inducing stimuli. Transfected Wehi-s cells constitutively overexpressing human hsp 70 or 27 were then examined for their resistance to apoptosis inducing by these drugs. Using the MTT assay, hsp 27 and 70 overexpressing cells exhibited an increased resistance to cell death when compared to the parental line. The parental line demonstrated features of apoptosis, that is, cell shrinkage and single- and double-strand DNA breaks. Taken together these results demonstrate that an increase in cellular levels of hsp 27 or 70, either by a mild heat shock treatment or by stable transfection, increases the resistance of U937 and Wehi-s cells to apoptotic cell death.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0014-4827
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
223
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
163-70
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Heat shock proteins increase resistance to apoptosis.
pubmed:affiliation
Department of Biochemistry, University College, Cork, Ireland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't