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Autocrine Fibroblast Growth Factor 2 Increases the Multipotentiality of Human Adipose‐Derived Mesenchymal Stem Cells
Author(s) -
Rider David A.,
Dombrowski Christian,
Sawyer Amber A.,
Ng Grace H. B.,
Leong David,
Hutmacher Dietmar W.,
Nurcombe Victor,
Cool Simon M.
Publication year - 2008
Publication title -
stem cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.159
H-Index - 229
eISSN - 1549-4918
pISSN - 1066-5099
DOI - 10.1634/stemcells.2007-0480
Subject(s) - mesenchymal stem cell , biology , stem cell transplantation for articular cartilage repair , stem cell , microbiology and biotechnology , adipogenesis , adipose tissue , cd146 , multipotent stem cell , bone marrow , wnt signaling pathway , adult stem cell , clinical uses of mesenchymal stem cells , immunology , cancer research , endothelial stem cell , cd34 , endocrinology , signal transduction , progenitor cell , in vitro , biochemistry
Multipotent mesenchymal stem cells (MSCs), first identified in the bone marrow, have subsequently been found in many other tissues, including fat, cartilage, muscle, and bone. Adipose tissue has been identified as an alternative to bone marrow as a source for the isolation of MSCs, as it is neither limited in volume nor as invasive in the harvesting. This study compares the multipotentiality of bone marrow‐derived mesenchymal stem cells (BMSCs) with that of adipose‐derived mesenchymal stem cells (AMSCs) from 12 age‐ and sex‐matched donors. Phenotypically, the cells are very similar, with only three surface markers, CD106, CD146, and HLA‐ABC, differentially expressed in the BMSCs. Although colony‐forming units‐fibroblastic numbers in BMSCs were higher than in AMSCs, the expression of multiple stem cell‐related genes, like that of fibroblast growth factor 2 (FGF2), the Wnt pathway effectors FRAT1 and frizzled 1, and other self‐renewal markers, was greater in AMSCs. Furthermore, AMSCs displayed enhanced osteogenic and adipogenic potential, whereas BMSCs formed chondrocytes more readily than AMSCs. However, by removing the effects of proliferation from the experiment, AMSCs no longer out‐performed BMSCs in their ability to undergo osteogenic and adipogenic differentiation. Inhibition of the FGF2/fibroblast growth factor receptor 1 signaling pathway demonstrated that FGF2 is required for the proliferation of both AMSCs and BMSCs, yet blocking FGF2 signaling had no direct effect on osteogenic differentiation. Disclosure of potential conflicts of interest is found at the end of this article.

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