ArticleFEBS open bio2019
Human amnion-derived mesenchymal stem cells promote osteogenesis of human bone marrow mesenchymal stem cells against glucolipotoxicity.
Article in FEBS open bio, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Characterisation and Expression of Osteogenic and Periodontal Markers of Bone Marrow Mesenchymal Stem Cells (BM-MSCs) from Diabetic Knee Joints.International journal of molecular sciences · 2024Article
- The Effect of Diabetes Mellitus on IGF Axis and Stem Cell Mediated Regeneration of the Periodontium.Bioengineering (Basel, Switzerland) · 2021Review
- Article
- Characteristics and Therapeutic Potential of Human Amnion-Derived Stem Cells.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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Registered trials
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