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    Please use this identifier to cite or link to this item: https://ir.fy.edu.tw:8080/ir/handle/987654321/8719

    Title: Advanced glycation end-product-inhibited cell proliferation and protein expression of beta-catenin and cyclin D1 are dependent on glycogen synthase kinase 3beta in LLC-PK1 cells.
    Authors: Lin, K.H.;Guh, J.Y.;Mo, J.F.;Chiou, S.J.;Hwang, C.C.;Chuang, L.Y.
    Contributors: 輔英科技大學 醫學檢驗生物技術系
    Date: 2008-09-01
    Issue Date: 2010-11-03 15:44:15 (UTC+8)
    Abstract: Glycogen synthase kinase 3beta (GSK3beta) is increased by high glucose in mesangial cells. Thus, we studied the role of GSK3beta in advanced glycation end-product (AGE)-induced effects in the proximal tubule-like LLC-PK1 cells. We found that AGE (100 microg/ml) time-dependently (8-48 h) increased phospho-GSK3beta-Tyr216 (active GSK3beta) and time-dependently (4-24 h) decreased phospho-GSK3beta-Ser21/9 (inactive GSK3beta) protein expression. Meanwhile, AGE (100 microg/ml) activated GSK3beta kinase at 8-48 h. AGE (100 microg/ml) dose-dependently (75-100 microg/ml) decreased beta-catenin protein expression but AGE did not decrease beta-catenin protein expression until 48 h. SB216763 (a GSK3beta inhibitor) and GSK3beta shRNA attenuated AGE (100 microg/ml)-inhibited cell proliferation and protein expression of beta-catenin and cyclin D1 at 48 h. SB216763 also attenuated AGE-induced type IV collagen. We conclude that AGE activates GSK3beta in LLC-PK1 cells. AGE-inhibited beta-catenin and cyclin D1 protein expression are dependent on GSK3beta. Moreover, AGE-inhibited cell proliferation and AGE-induced type IV collagen protein expression are dependent on GSK3beta.
    Relation: Archieve of Biochemistry and Biophysics 477(1),27-32
    Appears in Collections:[醫學檢驗生物技術系] 期刊論文

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