Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1993-3-4
pubmed:abstractText
Hemopoietic growth factors promote cell survival, proliferation and differentiation, but whether these processes, which often occur in concert, are mediated through the same or different receptor signaling mechanisms is not known. Using the bone marrow-derived IL-3-dependent cell line, 32D, we show that dibutyryl cyclic adenosine monophosphate (dbcAMP) retards the rapid loss of viable cells seen in the absence of IL-3. This effect is shown to be concentration-dependent and detectable within 16 hours of culture and is not associated with cell differentiation. At earlier times (2 to 7 hours), when no significant changes in cell numbers were observed, dbcAMP stimulated the reduction of dimethylthiazoldiphenyl tetrazolium bromide (MTT), and this effect was indistinguishable from that seen with IL-3. In contrast, control cells deprived of growth factor showed a decline in MTT response over this period. The effect of dbcAMP in maintaining cell viability and MTT responsiveness was associated with a concentration-dependent inhibition of 3H-thymidine incorporation into DNA, and retardation of the intranucleosomal cleavage of DNA that is associated with apoptosis. These results suggest that in 32D cells, cAMP can act to promote cell survival and retard apoptosis, quite independently of cell proliferation, by stimulating the activity of mitochondrial enzymes involved in MTT reduction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0301-472X
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
269-76
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Cyclic adenosine monophosphate promotes cell survival and retards apoptosis in a factor-dependent bone marrow-derived cell line.
pubmed:affiliation
Malaghan Institute of Medical Research, Wellington School of Medicine, Wellington Hospital, New Zealand.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't