Linked Life Data

10825236

Source:http://linkedlifedata.com/resource/pubmed/id/10825236

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-7-3
pubmed:abstractText
Transforming growth factor-beta1 (TGF-beta1) has been described as an efficient growth inhibitor that maintains the CD34(+) hematopoietic progenitor cells in quiescence. The concept of high proliferative potential-quiescent cells or HPP-Q cells has been introduced as a working model to study the effect of TGF-beta1 in maintaining the reversible quiescence of the more primitive hematopoietic stem cell compartment. HPP-Q cells are primitive quiescent stem/progenitor cells on which TGF-beta1 has downmodulated the cytokine receptors. These cells can be released from quiescence by neutralization of autocrine or endogenous TGF-beta1 with a TGF-beta1 blocking antibody or a TGF-beta1 antisense oligonucleotide. In nonhematopoietic systems, TGF-beta1 cooperates with the cyclin-dependent kinase inhibitor, p21(cip1), to induce cell cycle arrest. We therefore analyzed whether endogenous TGF-beta1 controls the expression of the p21(cip1) in the CD34(+) undifferentiated cells using a sensitive in situ hybridization method. We observed that addition of anti-TGF-beta1 is followed by a rapid decrease in the level of p21(cip1) mRNA whereas TGF-beta1 enhances p21(cip1) mRNA expression concurrently with an inhibitory effect on progenitor cell proliferation. These results suggest the involvement of p21(cip1) in the cell cycle control of early human hematopoietic quiescent stem/progenitors and not only in the differentiation of more mature myeloid cells as previously described. The modulation of p21(cip1) observed in response to TGF-beta1 allows us to further precise the working model of high proliferative potential-quiescent cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0021-9541
pubmed:author
pubmed:copyrightInfo
Copyright 2000 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
184
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
80-5
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10825236-Antigens, CD34, pubmed-meshheading:10825236-Cell Cycle, pubmed-meshheading:10825236-Cell Division, pubmed-meshheading:10825236-Cells, Cultured, pubmed-meshheading:10825236-Cyclin-Dependent Kinase Inhibitor p21, pubmed-meshheading:10825236-Cyclins, pubmed-meshheading:10825236-Enzyme Inhibitors, pubmed-meshheading:10825236-Fetal Blood, pubmed-meshheading:10825236-Gene Expression Regulation, pubmed-meshheading:10825236-Hematopoietic Stem Cells, pubmed-meshheading:10825236-Humans, pubmed-meshheading:10825236-Infant, Newborn, pubmed-meshheading:10825236-Kinetics, pubmed-meshheading:10825236-Oligodeoxyribonucleotides, Antisense, pubmed-meshheading:10825236-Recombinant Proteins, pubmed-meshheading:10825236-Transcription, Genetic, pubmed-meshheading:10825236-Transforming Growth Factor beta
pubmed:year
2000
pubmed:articleTitle
p21(cip1) mRNA is controlled by endogenous transforming growth factor-beta1 in quiescent human hematopoietic stem/progenitor cells.
pubmed:affiliation
Laboratoire de Biologie des Cellules Souches Somatiques Humaines, Centre National de la Recherche Scientifique (CNRS), Villejuif, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't