Brain and muscle aryl hydrocarbon receptor nuclear translocator-like protein-1 cooperates with glycogen synthase kinase-3β to regulate osteogenesis of bone-marrow mesenchymal stem cells in type 2 diabetes

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• 作者：Xiaoguang Li^a ; ¹ ; ^{xiaopa3084@126.com} ; Na Liu^a ; ¹ ; ^{liuna0216@163.com} ; Yizhu Wang^a ; ^{17701308150@163.com} ; Jinglong Liu^a ; ^{summer_mimosa@hotmail.com} ; Haigang Shi^b ; ^{402926405@qq.com} ; Zhenzhen Qu^c ; ^{quzhenzhen2008@126.com} ; Tingting Du^a ; ^{251697011@qq.com} ; Bin Guo^a ; ^{guobin0408@126.com} ; Bin Gu^a ; ^{gubmail@gmail.com}
• 关键词：Bone marrow mesenchymal stem cells ; Osteogenic differentiation ; Brain and muscle aryl hydrocarbon receptor nuclear translocator-like protein-1 ; Glycogen synthase kinase-3β ; Type 2 diabetes mellitus
• 刊名：Molecular and Cellular Endocrinology
• 出版年：2017
• 出版时间：15 January 2017
• 年：2017
• 卷：440
• 期：Complete
• 页码：93-105
• 全文大小：4315 K
• 卷排序：440

文摘

BMSCs osteogenesis is suppressed along with reduced BMAL1 and activated GSK3β in T2DM. BMAL1 downregulation inhibits Wnt/β-catenin pathway mainly via enhanced GSK3β in BMSCs. BMAL1 overexpression inhibits GSK-3β resulting in activation of Wnt/β-catenin pathway. GSK3β inhibition has a synergistic effect with overexpression of BMAL1 in GK BMSCs. Up-regulation of BMAL1 can recover the inhibited osteogenesis of BMSCs in T2DM.