2024-03-28T20:08:00Zhttps://eprints.lib.hokudai.ac.jp/dspace-oai/requestoai:eprints.lib.hokudai.ac.jp:2115/656612022-11-17T02:08:08Zhdl_2115_20043hdl_2115_137Depletion of Gangliosides Enhances Articular Cartilage Repair in MiceMatsuoka, MasatakeOnodera, TomohiroHoman, KentaroSasazawa, FumioFurukawa, Jun-ichiMomma, DaisukeBaba, RikiyaHontani, KazutoshiJoutoku, ZentaMatsubara, ShinjiYamashita, TadashiIwasaki, Norimasa490Elucidation of the healing mechanisms in damaged tissues is a critical step for establishing breakthroughs in tissue engineering. Articular cartilage is clinically one of the most successful tissues to be repaired with regenerative medicine because of its homogeneous extracellular matrix and few cell types. However, we only poorly understand cartilage repair mechanisms, and hence, regenerated cartilage remains inferior to the native tissues. Here, we show that glycosylation is an important process for hypertrophic differentiation during articular cartilage repair. GM3, which is a precursor molecule for most gangliosides, was transiently expressed in surrounding damaged tissue, and depletion of GM3 synthase enhanced cartilage repair. Gangliosides also regulated chondrocyte hypertrophy via the Indian hedgehog pathway. These results identify a novel mechanism of cartilage healing through chondrocyte hypertrophy that is regulated by glycosylation. Manipulation of gangliosides and their synthases may have beneficial effects on articular cartilage repair.Nature Publishing GroupJournal Articleapplication/pdfapplication/pdfhttp://hdl.handle.net/2115/65661https://eprints.lib.hokudai.ac.jp/dspace/bitstream/2115/65661/2/srep43729-s1.pdfhttps://eprints.lib.hokudai.ac.jp/dspace/bitstream/2115/65661/1/srep43729.pdf2045-2322Scientific reports7437292017-03-02enginfo:doi/10.1038/srep43729http://creativecommons.org/licenses/by/4.0/publisher