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Erschienen in: Journal of Bone and Mineral Metabolism 2/2016

01.03.2016 | Original Article

High glucose microenvironments inhibit the proliferation and migration of bone mesenchymal stem cells by activating GSK3β

verfasst von: Bo Zhang, Na Liu, Haigang Shi, Hao Wu, Yuxuan Gao, Huixia He, Bin Gu, Hongchen Liu

Erschienen in: Journal of Bone and Mineral Metabolism | Ausgabe 2/2016

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Abstract

Diabetes mellitus involves metabolic changes that can impair bone repair. Bone mesenchymal stem cells (BMSCs) play an important role in bone regeneration. However, the bone regeneration ability of BMSCs is inhibited in high glucose microenvironments. It can be speculated that this effect is due to changes in BMSCs' proliferation and migration ability, because the recruitment of factors with an adequate number of MSCs and the microenvironment around the site of bone injury are required for effective bone repair. Recent genetic evidence has shown that the Cyclin D1 and the CXC receptor 4 (CXCR-4) play important roles in the proliferation and migration of BMSCs. In this study we determined the specific role of glycogen synthase kinase-3β (GSK3β) in the proliferation and migration of BMSCs in high glucose microenvironments. The proliferation and migration ability of BMSCs were suppressed under high glucose conditions. We showed that high glucose activates GSK3β but suppresses CXCR-4, β-catenin, LEF-1, and cyclin D1. Inhibition of GSK3β by LiCl led to increased levels of β-catenin, LEF-1, cyclin D1, and CXCR-4 expression. Our data indicate that GSK3β plays an important role in regulating the proliferation and migration of BMSCs by inhibiting cyclin D1 and CXCR-4 under high glucose conditions.
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Metadaten
Titel
High glucose microenvironments inhibit the proliferation and migration of bone mesenchymal stem cells by activating GSK3β
verfasst von
Bo Zhang
Na Liu
Haigang Shi
Hao Wu
Yuxuan Gao
Huixia He
Bin Gu
Hongchen Liu
Publikationsdatum
01.03.2016
Verlag
Springer Japan
Erschienen in
Journal of Bone and Mineral Metabolism / Ausgabe 2/2016
Print ISSN: 0914-8779
Elektronische ISSN: 1435-5604
DOI
https://doi.org/10.1007/s00774-015-0662-6

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