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. 2020 Mar 31;10:5722. doi: 10.1038/s41598-020-62580-0

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Cell distribution of transplanted cartilage gels in a non-human primate cartilage defect model after 24 weeks. (A) Representative RT-PCR result bio-distribution using human specific Alu sequence. Human Alu was detected in the transplanted cartilage tissue and was absent in adjacent tibial cartilage, synovium, and other vital organs. (B) Cell tracking using human anti-nuclear antibody. Immunohistochemical staining results showed that cartilage gels of human origin remained within the defect after 24 weeks. Safranin-O slide shown as reference for repair site. (C) Semi-quantification of immunohistochemistry results showed over 50% of human anti-nuclear antibody (+) cells within the defect. Statistical analysis done with Mann-Whitney test (*p < 0.05, **p < 0.01, ***p < 0.001). Magnification x40. FCPC; fetal cartilage progenitor cells, TK; transplanted knee, NHP; non-human primate, HuNu; human anti-nuclear antibody, FOV; field of view (x40).