Advanced glycation end-product-inhibited cell proliferation and protein expression of beta-catenin and cyclin D1 are dependent on glycogen synthase kinase 3 beta in LLC-PK1 cells

[摘要]：Glycogen synthase kinase 3 beta (GSK3 beta) is increased by high glucose in mesangial cells. Thus, we studied the role of GSK3 beta in advanced glycation end-product (AGE)-induced effects in the proximal tubule-like LLC-PK1 cells. We found that AGE (100 mu g/ml) time-dependently (8-48 h) increased phospho-GSK3 beta-Tyr216 (active GSK3 beta) and time-dependently (4-24 h) decreased phospho-GSK3 beta-Ser21/9 (inactive GSK3 beta) protein expression. Meanwhile, AGE (100 mu g/ml) activated GSK3 beta kinase at 8-48h. AGE (100 mu g/ml) dose-dependently (75-100 mu g/ml) decreased beta-catenin protein expression but AGE did not decrease beta-catenin protein expression until 48 h. SB216763 (a GSK3 beta inhibitor) and GSK3 beta shRNA attenuated AGE (100 mu g/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 GSK3 beta in LLC-PK1 cells. AGE-inhibited beta-catenin and cyclin D1 protein expression are dependent on GSK3 beta. Moreover, AGE-inhibited cell proliferation and AGE-induced type IV collagen protein expression are dependent on GSK3 beta. (c) 2008 Elsevier Inc. All rights reserved.

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