Macromolecular Bioscience
Macromolecular Bioscience
4 years ago

Maintenance of Cartilaginous Gene Expression of Serially Subcultured Chondrocytes on Poly(2-Methoxyethyl Acrylate) Analogous Polymers

Maintenance of Cartilaginous Gene Expression of Serially Subcultured Chondrocytes on Poly(2-Methoxyethyl Acrylate) Analogous Polymers
Chiho Endo, Guoping Chen, Takashi Hoshiba, Hiroka Maruyama, Masaru Tanaka, Naoki Kawazoe, Kazuhiro Sato
Chondrocytes are important for cartilage tissue engineering. However, dedifferentiation during chondrocyte subculture prevents the application of cartilage tissue engineering. Therefore, prevention of this dedifferentiation is required. Here, the possibility of poly(2-methoxyethyl acrylate) (PMEA) and its analogous polymers, poly(tetrahydrofurfuryl acrylate) (PTHFA) and poly(2-(2-methoxyethoxy) ethyl acrylate-co-butyl acrylate) (PMe2A), for chondrocyte subculture without dedifferentiation is examined. Chondrocytes spread on PTHFA and polyethylene terephthalate (PET), whereas their spreading is delayed on PMEA and PMe2A. When primary chondrocytes are subcultured on these polymers, the expression levels of cartilaginous genes are higher on PMEA and PMe2A than on PET and PTHFA. Integrin contribution to the initial cell adhesion is lower on PMEA and PMe2A than on PTHFA and PET. This low level of integrin contribution to cell adhesion may cause a delay in cell spreading and the maintenance of cartilaginous gene expression. These results indicate that PMEA and PMe2A may be favorable substrates for chondrocyte subculture and cartilage tissue engineering. Chondrocytes are subcultured on the substrates coated with poly(2-methoxyethyl acrylate) (PMEA) and its analogs that can suppress protein adsorption. The cells can adhere on PMEA analogs through both integrin-dependent and -independent mechanisms. And the integrin α5-mediated adhesion is suppressed after the culture. Finally, the cells maintain their specific gene expression during the subculture through the suppression of cell spreading.

Publisher URL: http://onlinelibrary.wiley.com/resolve/doi

DOI: 10.1002/mabi.201700297

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