Ikeda, YasutoshiSakaue, MoritoChijimatsu, RyotaHart, David A.Otsubo, HidenoriShimomura, KazunoriMadry, HenningSuzuki, TomoyukiYoshikawa, HidekiYamashita, ToshihikoNakamura, Norimasa2018-09-272018-09-272017-06-27Yasutoshi Ikeda, Morito Sakaue, Ryota Chijimatsu, et al., “IGF-1 Gene Transfer to Human Synovial MSCs Promotes Their Chondrogenic Differentiation Potential without Induction of the Hypertrophic Phenotype,” Stem Cells International, vol. 2017, Article ID 5804147, 10 pages, 2017. doi:10.1155/2017/5804147http://dx.doi.org/10.1155/2017/5804147http://hdl.handle.net/1880/108081Mesenchymal stem cell- (MSC-) based therapy is a promising treatment for cartilage. However, repair tissue in general fails to regenerate an original hyaline-like tissue. In this study, we focused on increasing the expression levels for insulin-like growth factor-1 (IGF-1) to improve repair tissue quality. The IGF-1 gene was introduced into human synovial MSCs with a lentiviral vector and examined the levels of gene expression and morphological status of MSCs under chondrogenic differentiation condition using pellet cultures. The size of the pellets derived from IGF-1-MSCs were significantly larger than those of the control group. The abundance of glycosaminoglycan (GAG) was also significantly higher in the IGF-1-MSC group. The histology of the IGF-1-induced pellets demonstrated similarities to hyaline cartilage without exhibiting features of a hypertrophic chondrocyte phenotype. Expression levels for the Col2A1 gene and protein were significantly higher in the IGF-1 pellets than in the control pellets, but expression levels for Col10, MMP-13, ALP, and Osterix were not higher. Thus, IGF-1 gene transfer to human synovial MSCs led to an improved chondrogenic differentiation capacity without the detectable induction of a hypertrophic or osteogenic phenotype.Journal Article2018-09-27enCopyright © 2017 Yasutoshi Ikeda et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.10.11575/PRISM/33017