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Mol Cell Endocrinol. 2017 Jan 15;440:93-105. doi: 10.1016/j.mce.2016.10.001. Epub 2016 Oct 4.

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.

Author information

1
Institution of Stomatology, The General Hospital of Chinese PLA, Beijing, China. Electronic address: xiaopa3084@126.com.
2
Institution of Stomatology, The General Hospital of Chinese PLA, Beijing, China. Electronic address: liuna0216@163.com.
3
Institution of Stomatology, The General Hospital of Chinese PLA, Beijing, China. Electronic address: 17701308150@163.com.
4
Institution of Stomatology, The General Hospital of Chinese PLA, Beijing, China. Electronic address: summer_mimosa@hotmail.com.
5
Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, Beijing, China. Electronic address: 402926405@qq.com.
6
Department of Stomatology, Beijing Xinhua Hospital, Beijing, China. Electronic address: quzhenzhen2008@126.com.
7
Institution of Stomatology, The General Hospital of Chinese PLA, Beijing, China. Electronic address: 251697011@qq.com.
8
Institution of Stomatology, The General Hospital of Chinese PLA, Beijing, China. Electronic address: guobin0408@126.com.
9
Institution of Stomatology, The General Hospital of Chinese PLA, Beijing, China. Electronic address: gubmail@gmail.com.

Abstract

Type 2 diabetes mellitus (T2DM) is associated with inhibited osteogenesis of bone marrow mesenchymal stem cells (BMSCs). Brain and muscle ARNT-like protein 1 (BMAL1) has been linked to the T2DM-related bone remodeling, however, the specific mechanism is still unclear. Herein, we aimed to determine the role of BMAL1 in T2DM-induced suppression of BMSCs osteogenesis. Inhibited osteogenesis and BMAL1 expression were showed in diabetic BMSCs. And while β-catenin and T cell factor (TCF) expression were decreased, the glycogen synthase kinase-3β (GSK-3β) and nemo-like kinase (NLK) expression were increased in diabetic BMSCs. Moreover, over-expression of BMAL1 led to recovered osteogenesis ability and activation of Wnt/β-catenin pathway, which was partially due to inhibition of GSK-3β caused by over-expression of BMAL1. Taken together, our findings provide new insights into the role of BMAL1 in T2DM-induced suppression of BMSCs osteogenesis. Over-expressed BMAL1 could recover BMSCs osteogenesis in T2DM partially by decreasing GSK-3β expression to activate Wnt/β-catenin pathway. BMAL1 may have a potential use in repairing diabetic bone metabolic disorders.

KEYWORDS:

Bone marrow mesenchymal stem cells; Brain and muscle aryl hydrocarbon receptor nuclear translocator-like protein-1; Glycogen synthase kinase-3β; Osteogenic differentiation; Type 2 diabetes mellitus

PMID:
27717746
DOI:
10.1016/j.mce.2016.10.001
[Indexed for MEDLINE]

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