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  • Title: Increased proliferation of human synovial mesenchymal stem cells with autologous human serum: comparisons with bone marrow mesenchymal stem cells and with fetal bovine serum.
    Author: Nimura A, Muneta T, Koga H, Mochizuki T, Suzuki K, Makino H, Umezawa A, Sekiya I.
    Journal: Arthritis Rheum; 2008 Feb; 58(2):501-10. PubMed ID: 18240254.
    Abstract:
    OBJECTIVE: Synovial mesenchymal stem cells (MSCs) are a promising cell source for cartilage regeneration due to their high chondrogenic potential. For clinical safety, autologous human serum should be used instead of fetal bovine serum (FBS). We undertook this study to compare the 2 types of serum for their enhancement of the proliferation and chondrogenic potentials of synovial MSCs and to investigate the mechanisms of the differences. Since effectiveness of the sera might depend on the origin of the MSCs, we also examined bone marrow MSCs. METHODS: Synovium, bone marrow, and peripheral blood were obtained from 18 donors. Synovial and bone marrow MSCs were cultured with autologous human serum or FBS and analyzed. In addition, rabbit synovial MSCs cultured with autologous serum or FBS were transplanted into full-thickness cartilage defects of the knees of the same rabbits. RESULTS: Human synovial MSCs expanded more in human serum than in FBS, and the opposite results were obtained with bone marrow MSCs. Hierarchical clustering analysis showed that the cell source, rather than the type of serum, affected the gene expression profile. Human serum contained high levels of platelet-derived growth factor (PDGF), synovial MSCs expressed higher levels of PDGF receptor alpha than did bone marrow MSCs, and neutralizing PDGF decreased the proliferation of synovial MSCs with autologous human serum. Although the in vitro chondrogenic potential of human synovial MSCs was affected by the serum source, the in vivo chondrogenic potential of rabbit synovial MSCs was similar in autologous serum and FBS groups. CONCLUSION: Autologous serum predominates in increasing the proliferation of synovial MSCs with chondrogenic potential through PDGF signaling.
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