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논문 기본 정보

자료유형
학술저널
저자정보
Shin, Dong-Wook (Skin Research Institute, AmorePacific Corporation R&D Center) Shim, Joong-Hyun (Skin Research Institute, AmorePacific Corporation R&D Center) Kim, Yoon-Kyung (Skin Research Institute, AmorePacific Corporation R&D Center) Son, Eui-Dong (Skin Research Institute, AmorePacific Corporation R&D Center) Yang, Seung-Ha (Skin Research Institute, AmorePacific Corporation R&D Center) Jeong, Hye-Jin (Skin Research Institute, AmorePacific Corporation R&D Center) Lee, Seok-Yong (Department of Pharmacy, Sungkyunkwan University) Kim, Han-Kon (Department of Pharmacy, Sungkyunkwan University) Park, Soo-Nam (Department of Fine Chemistry, College of Nature and Life Science, Seoul National University of Technology) Noh, Min-Soo (Skin Research Institute, AmorePacific Corporation R&D Center)
저널정보
한국응용약물학회 Biomolecules & Therapeutics(구 응용약물학회지) Biomolecules & therapeutics 제18권 제3호
발행연도
2010.1
수록면
280 - 285 (6page)

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Glycosaminoglycans (GAGs) and chitosan have been used as matrix materials to support the dermal part of skin equivalent which is used for both pharmacological and toxicological evaluations of drugs potentially used for dermatological diseases. However, their biological roles of GAGs and chitosan in the skin equivalent are still unknown. In the present study, we evaluated whether GAGs and chitosan directly affect keratinocyte stem cells (KSCs) and their transit-amplifying cells (TA cells). Among supporting matrix materials, chitosan significantly increased the number of ${\alpha}6$ $integrin^{high}/CD71^{high}$ human keratinocyte TA cells by 48.5%. In quantitative real-time RT-PCR analysis, chitosan significantly increased CD71 and CD200 gene transcription whereas not ${\alpha}6$ integrin. In addition, the level of the gene transcription of both keratin 1 (K1) and K10 in the chitosan-treated human keratinocytes was significantly lower than those of control, suggesting that chitosan inhibit keratinocyte differentiation. We also found that N-acetyl-D-glucosamine (NAG) and $\beta$-(1-4)-linked D-glucosamine (D-glc), two components of chitosan, have no effect on the expression of CD71, K1, and K10, suggesting that each monomer component of chitosan is not enough to regulate the number of epidermal keratinocyte lineage. Conclusively, chitosan increases keratinocyte TA cell population which may contribute to the cellular mass expansion of the epidermal part of a skin equivalent system.

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