ArticleJournal of bone and mineral metabolism2016
High glucose microenvironments inhibit the proliferation and migration of bone mesenchymal stem cells by activating GSK3β.
Article in Journal of bone and mineral metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed.
- Melatonin improves osteogenic differentiation in a high-glucose environment by activating NRF2 to promote autophagy through the regulation of cross-talk between macrophages and bone marrow mesenchymal stem cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Biomaterial regulation of excessive inflammation restores osteoimmune homeostasis in diabetic bone regeneration.Regenerative biomaterials · 2026Review
- piRNA DQ690018 increased bone mass by promoting the proliferation and osteogenic differentiation of BMSCs.Journal of orthopaedic surgery and research · 2025Article
- Effects of low glucose microenvironment on the proliferation, migration and senescence of meniscus-derived stem cells.Scientific reports · 2025Article
- Comparison of Differences in Cell Migration during the Osteogenic and Adipogenic Differentiation of the Bone Marrow-Derived Stem Cells.Journal of bone metabolism · 2025Article
- High glucose induces senescence in synovial mesenchymal stem cells through mitochondrial dysfunction.BMC oral health · 2025Article
- Addressing the challenges of infectious bone defects: a review of recent advances in bifunctional biomaterials.Journal of nanobiotechnology · 2025Review
- MiR-146a Is Mutually Regulated by High Glucose-Induced Oxidative Stress in Human Periodontal Ligament Cells.International journal of molecular sciences · 2024Article
- Gestational diabetes mellitus affects the differentiation of hematopoietic stem cells in neonatal umbilical cord blood.Archives of gynecology and obstetrics · 2024Article
- High glucose microenvironment and human mesenchymal stem cell behavior.World journal of stem cells · 2024Article
- 3D printing and bioprinting in the battle against diabetes and its chronic complications.Frontiers in bioengineering and biotechnology · 2024Review
- Evaluate the effects of low-intensity pulsed ultrasound on dental implant osseointegration under type II diabetes.Frontiers in bioengineering and biotechnology · 2024Article
- Osteogenesis of bone marrow mesenchymal stem cell in hyperglycemia.Frontiers in endocrinology · 2023Review
- Iron metabolism and ferroptosis in diabetic bone loss: from mechanism to therapy.Frontiers in nutrition · 2023Review
- Article
- Enamel matrix derivative expedites osteogenic differentiation of BMSCs via Wnt/β-catenin pathway in high glucose microenvironment.Journal of bone and mineral metabolism · 2022Article
- Ginsenoside Rb1 Modulates the Migration of Bone-Derived Mesenchymal Stem Cells through the SDF-1/CXCR4 Axis and PI3K/Akt Pathway.Disease markers · 2022Article
- Challenges to Improve Bone Healing Under Diabetic Conditions.Frontiers in endocrinology · 2022Review
- Effectiveness and Mechanisms of Low-Intensity Pulsed Ultrasound on Osseointegration of Dental Implants and Biological Functions of Bone Marrow Mesenchymal Stem Cells.Stem cells international · 2022Review
- Curcumin Prevents Diabetic Osteoporosis through Promoting Osteogenesis and Angiogenesis Coupling via NF-Evidence-based complementary and alternative medicine : eCAM · 2022Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
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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