Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1996-9-12
pubmed:abstractText
The expression of c-myc was analyzed in murine and human erythroblasts throughout their differentiation in vitro into reticulocytes. The murine cells were splenic erythroblasts from animals infected with the anemia strain of Friend virus (FVA cells). In FVA cells cultured without EPO, the c-myc mRNA and protein levels decrease sharply within 3 to 4 h, showing that continual EPO stimulation is required to maintain c-myc expression. When cultured with EPO, the c-myc mRNA level of FVA cells is raised within 30 min of exposure. The c-myc mRNA and protein reach maxima at 1 to 3 h, then decline slowly to very low levels by 18 h. In contrast, c-fos and c-jun mRNA levels are not regulated by EPO in FVA cells. The human cells analyzed were colony-forming units-erythroid, CFU-E, derived in vitro by the culture of peripheral blood burst-forming units-erythroid (BFU-E). When grown in EPO and insulin-like growth factor 1 (IGF-1) these cells differentiate into reticulocytes over 6 days rather than the 2 days required for murine cells, but the c-myc mRNA kinetics and response to EPO parallel those of mouse cells at similar stages of differentiation. Both IGF-1 and c-kit ligand (SCF) cause an additive increase in c-myc mRNA in human CFU-E in conjunction with EPO. These additive effects suggest that EPO, IGF-1, and SCF affect c-myc mRNA accumulation by distinct mechanisms. Addition of an antisense oligonucleotide to c-myc in cultures of human CFU-E specifically inhibited cell proliferation but did not affect erythroid cell differentiation or apoptosis. When human cells were grown in high SCF concentrations, an environment which enhances proliferation and retards differentiation, antisense oligonucleotide to c-myc strongly inhibited proliferation, but such inhibition did not induce differentiation. This latter result indicates that differentiation requires signals other than depression of c-Myc and resultant depression of proliferation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0021-9541
pubmed:author
pubmed:issnType
Print
pubmed:volume
168
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
255-63
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:8707861-Animals, pubmed-meshheading:8707861-Base Sequence, pubmed-meshheading:8707861-Cell Division, pubmed-meshheading:8707861-Cell Survival, pubmed-meshheading:8707861-DNA Probes, pubmed-meshheading:8707861-Electrophoresis, Polyacrylamide Gel, pubmed-meshheading:8707861-Erythroblasts, pubmed-meshheading:8707861-Erythroid Precursor Cells, pubmed-meshheading:8707861-Erythropoietin, pubmed-meshheading:8707861-Friend murine leukemia virus, pubmed-meshheading:8707861-Gene Expression Regulation, Developmental, pubmed-meshheading:8707861-Genes, myc, pubmed-meshheading:8707861-Humans, pubmed-meshheading:8707861-Insulin-Like Growth Factor I, pubmed-meshheading:8707861-Iron, pubmed-meshheading:8707861-Mice, pubmed-meshheading:8707861-Molecular Sequence Data, pubmed-meshheading:8707861-Oligonucleotides, Antisense, pubmed-meshheading:8707861-Proto-Oncogene Proteins c-myc, pubmed-meshheading:8707861-RNA, Messenger, pubmed-meshheading:8707861-Stem Cell Factor
pubmed:year
1996
pubmed:articleTitle
C-myc expression affects proliferation but not terminal differentiation or survival of explanted erythroid progenitor cells.
pubmed:affiliation
Department of Medicine, Department of Veterans Affairs Medical Center, Nashville, Tennessee, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.