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Vol. 16, Issue 3, 1131-1141, March 2005
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* Institute of Basic Medical Sciences, University of Oslo, 0317 Oslo, Norway;
Institute of Immunology, Rikshospitalet University Hospital, 0027 Oslo, Norway; and
Centre for Occupational and Environmental Medicine, Rikshospitalet University Hospital, 0027 Oslo, Norway
Submitted November 1, 2004;
Accepted December 13, 2004
Monitoring Editor: Carl-Henrik Heldin
Stromal stem cells proliferate in vitro and may be differentiated along several lineages. Freshly isolated, these cells have been too few or insufficiently pure to be thoroughly characterized. Here, we have isolated two populations of CD45-CD34+CD105+ cells from human adipose tissue which could be separated based on expression of CD31. Compared with CD31+ cells, CD31- cells overexpressed transcripts associated with cell cycle quiescence and stemness, and transcripts involved in the biology of cartilage, bone, fat, muscle, and neural tissues. In contrast, CD31+ cells overexpressed transcripts associated with endothelium and the major histocompatibility complex class II complex. Clones of CD31- cells could be expanded in vitro and differentiated into cells with characteristics of bone, fat, and neural-like tissue. On culture, transcripts associated with cell cycle quiescence, stemness, certain cytokines and organ specific genes were down-regulated, whereas transcripts associated with signal transduction, cell adhesion, and cytoskeletal components were up-regulated. CD31+ cells did not proliferate in vitro. CD45-CD34+CD105+CD31- cells from human adipose tissue have stromal stem cell properties which may make them useful for tissue engineering.
Abbreviations used: ADASC, adipose tissue-derived adult stem cells; MSC, mesenchymal stem cells; CFU-F, colony-forming units-fibroblasts; SVF, stromal vascular fraction; ECM, extracellular matrix; HSC, hematopoietic stem cells; NGFR, nerve growth factor receptor.
The online version of this article contains supplemental material at MBC Online (http://www.molbiolcell.org).
These authors contributed equally to this work.
Address correspondence to: Jan E. Brinchmann (j.e.brinchmann{at}labmed.uio.no) or Philippe Collas (philippe.collas{at}medisin.uio.no).
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