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FGF‐2 enhances the mitotic and chondrogenic potentials of human adult bone marrow‐derived mesenchymal stem cells
Author(s) -
Solchaga Luis A.,
Penick Kitsie,
Porter John D.,
Goldberg Victor M.,
Caplan Arnold I.,
Welter Jean F.
Publication year - 2005
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.20238
Subject(s) - mesenchymal stem cell , microbiology and biotechnology , chondrogenesis , fibroblast growth factor , extracellular matrix , stem cell , biology , proteoglycan , cellular differentiation , chemistry , gene , genetics , receptor
Abstract Human mesenchymal stem cells (hMSCs) expanded with and without fibroblast growth factor (FGF) supplementation were compared with respect to their proliferation rate, ability to differentiate along the chondrogenic pathway in vitro, and their gene expression profiles. hMSCs expanded in FGF‐supplemented medium were smaller and proliferated more rapidly than hMSCs expanded in control conditions. Chondrogenic cultures made with FGF‐treated cells were larger and contain more proteoglycan than those made with control cells. Furthermore, aggregates of FGF‐treated cells lacked the collagen type I‐positive and collagen type II‐negative outer layer characteristic of aggregates of control cells. A total of 358 unique transcripts were differentially expressed in FGF‐treated hMSCs. Of these, 150 were upregulated and 208 downregulated. Seventeen percent of these genes affect proliferation. Known genes associated with cellular signaling functions comprised the largest percentage (∼20%) of differentially expressed transcripts. Eighty percent of differentially expressed extracellular matrix‐related genes were downregulated. The present findings that FGF‐2 enhances proliferation and differentiation of hMSCs adds to a growing body of evidence that cytokines modulate the differentiation potential and, perhaps, the multipotentiality of adult stem cells. With the generation of gene expression profiles of FGF‐treated and control cells we have taken the first steps in the elucidation of the molecular mechanism(s) behind these phenomena. © 2004 Wiley‐Liss, Inc.