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Human amnion‐derived mesenchymal stem cells promote osteogenesis of human bone marrow mesenchymal stem cells against glucolipotoxicity
Epidemiological evidence suggests that diabetes mellitus (DM) is an important factor in promoting periodontitis. It not only affects the attachment of connective tissue but also causes loss of alveolar bone. Hence, there is an urgent need to find an effective treatment for DM‐induced bone deficiency...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6325622/ https://www.ncbi.nlm.nih.gov/pubmed/30652075 http://dx.doi.org/10.1002/2211-5463.12547 |
Sumario: | Epidemiological evidence suggests that diabetes mellitus (DM) is an important factor in promoting periodontitis. It not only affects the attachment of connective tissue but also causes loss of alveolar bone. Hence, there is an urgent need to find an effective treatment for DM‐induced bone deficiency. This study aimed to investigate the effects of human amniotic mesenchymal stem cells (HAMSCs) on the proliferation and osteogenic differentiation of DM‐induced human bone marrow mesenchymal stem cells (HBMSCs). High glucose and palmitic acid (GP) were used to mimic DM‐induced glucolipotoxicity. The proliferation levels were measured using flow cytometry. Alkaline phosphatase activity substrate assays, Alizarin red S staining, and western blotting were used to investigate osteogenic differentiation. Oxidative stress was measured by assaying the levels of reactive oxygen species. This study found that glucolipotoxicity caused by GP remarkably inhibited cell proliferation and osteogenesis, and upregulated the oxidative stress level in HBMSCs. However, HAMSCs attenuated HBMSC dysfunction through antioxidant activity by influencing p38 mitogen‐activated protein kinase and vascular endothelial growth factor secretion. In conclusion, our findings indicate that HAMSCs might be suitable for treating DM‐mediated bone deficiency. |
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