Source:http://linkedlifedata.com/resource/pubmed/id/17375123
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
|
| pubmed:dateCreated |
2007-3-21
|
| pubmed:abstractText |
Type I interferon (IFN) is shown to control the reversible quiescence of a primitive human bone marrow mesenchymal stem cell (MSC) subpopulation. A 24 h pre-treatment of Stro1+/GlycoA- or CD45-/GlycoA- subpopulations with a monoclonal antibody (mAb) against the IFNAR1 chain of the human type I IFN receptor (64G12), or with a polyclonal anti-IFNalpha antibody, resulted in a marked increase in the number of very large colonies (CFU-F >3000 cells) obtained in the presence of low, but necessary, concentrations of bFGF. Over a 2-month culture period, this short activation promoted a faster and greater amplification of mesenchymal progenitors for adipocytes and osteoblasts. Activation correlated with inhibition of STAT1 and STAT2 phosphorylation and of STAT1 nuclear translocation. A non-neutralizing anti-IFNAR1 mAb was ineffective. We demonstrate that control and activated MSCs express ST3GAL3, a sialyltransferase necessary to produce the embryonic antigens SSEA-3 and -4. Interestingly, activated MSC progeny expressed SSEA-3 and -4 at a higher level than control cultures, but this was not correlated with a significant expression of other embryonic markers. As MSCs represent an essential tool in tissue regeneration, the use of 64G12, which rapidly recruits a higher number of primitive cells, might increase amplification safety for cell therapy.
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| pubmed:commentsCorrections | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Apr
|
| pubmed:issn |
0887-6924
|
| pubmed:author |
pubmed-author:BarberPP,
pubmed-author:CharbordPP,
pubmed-author:FortunelNN,
pubmed-author:HatzfeldAA,
pubmed-author:HatzfeldJJ,
pubmed-author:HaydontVV,
pubmed-author:LiJ CJC,
pubmed-author:LiM LML,
pubmed-author:MilovTT,
pubmed-author:MonierM-NMN,
pubmed-author:OostendorpR A JRA,
pubmed-author:PeifferII,
pubmed-author:ToveyMM
|
| pubmed:issnType |
Print
|
| pubmed:volume |
21
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
714-24
|
| pubmed:dateRevised |
2007-10-30
|
| pubmed:meshHeading |
pubmed-meshheading:17375123-Bone Marrow Cells,
pubmed-meshheading:17375123-Cell Culture Techniques,
pubmed-meshheading:17375123-Cell Differentiation,
pubmed-meshheading:17375123-Cell Division,
pubmed-meshheading:17375123-Colony-Forming Units Assay,
pubmed-meshheading:17375123-DNA Primers,
pubmed-meshheading:17375123-Extracellular Matrix,
pubmed-meshheading:17375123-Humans,
pubmed-meshheading:17375123-Immunophenotyping,
pubmed-meshheading:17375123-Interferon-alpha,
pubmed-meshheading:17375123-Interferon-beta,
pubmed-meshheading:17375123-Kinetics,
pubmed-meshheading:17375123-Mesenchymal Stem Cells,
pubmed-meshheading:17375123-Polymerase Chain Reaction,
pubmed-meshheading:17375123-Transforming Growth Factor beta1
|
| pubmed:year |
2007
|
| pubmed:articleTitle |
A sub-population of high proliferative potential-quiescent human mesenchymal stem cells is under the reversible control of interferon alpha/beta.
|
| pubmed:affiliation |
CNRS Human Stem Cell Laboratory, rue Guy Moquet, Villejuif, France. hatzfeld@vjf.cnrs.fr
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|