Source:http://linkedlifedata.com/resource/pubmed/id/12482505
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
2002-12-16
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pubmed:abstractText |
Bone marrow from wild-type mice and mice with mutated Fas (lpr) or mutated Fas ligand (gld) was used to investigate the role of the Fas/FasL system in the regulation of myeloid progenitor cell kinetics.Granulocyte-macrophage colony-forming cells (CFU-GM) were measured by a standard colony assay and the proliferative activity of CFU-GM was measured by replating primary colonies and observing secondary colony formation. Fas expression was restored to lpr mouse bone marrow cells by retrovirus-mediated gene transfer and gld mouse marrow cells were treated with soluble FasL. Wild-type marrow cells were treated with YVAD (a caspase inhibitor) or anti-Fas monoclonal antibodies. There were greater frequencies of myeloid progenitor cells (CFU-GM) in lpr and gld mouse marrow compared to wild-type (WT) marrow (p = 0.0008). The proliferative capacity of CFU-GM was also significantly greater for lpr and gld CFU-GM compared to WT CFU-GM (p = 0.0003 and 0.0001, respectively). Retrovirus-mediated restoration of Fas into lpr marrow, and provision of soluble FasL (sFasL) to gld CFU-GM reduced CFU-GM proliferation to WT levels. Treatment of WT CFU-GM with YVAD or anti-FasL monoclonal antibody increased CFU-GM proliferation to the levels found in lpr and gld CFU-GM. YVAD significantly increased and anti-Fas significantly reduced the proliferative capacity of human CFU-GM (p = 0.015 and 0.04, respectively).Fas, FasL, and caspase activation may play an important role in regulating myeloid progenitor cell kinetics.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/Caspases,
http://linkedlifedata.com/resource/pubmed/chemical/FASLG protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Fas Ligand Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Fasl protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0301-472X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
30
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1428-35
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pubmed:dateRevised |
2009-11-3
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pubmed:meshHeading |
pubmed-meshheading:12482505-Animals,
pubmed-meshheading:12482505-Antigens, CD95,
pubmed-meshheading:12482505-Apoptosis,
pubmed-meshheading:12482505-Bone Marrow Cells,
pubmed-meshheading:12482505-Caspases,
pubmed-meshheading:12482505-Cell Division,
pubmed-meshheading:12482505-Fas Ligand Protein,
pubmed-meshheading:12482505-Humans,
pubmed-meshheading:12482505-Kinetics,
pubmed-meshheading:12482505-Membrane Glycoproteins,
pubmed-meshheading:12482505-Mice,
pubmed-meshheading:12482505-Mice, Knockout,
pubmed-meshheading:12482505-Myeloid Progenitor Cells,
pubmed-meshheading:12482505-Transduction, Genetic
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pubmed:year |
2002
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pubmed:articleTitle |
A role for the Fas/Fas ligand apoptotic pathway in regulating myeloid progenitor cell kinetics.
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pubmed:affiliation |
LRF Centre For Adult Leukaemia, Department of Haematology, Faculty of Medicine, Imperial College of Science, Technology and Medicine, Hammersmith Campus, DuCane Road, London W12 0NN, UK.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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