Zinc is the second most abundant trace element in the human body, stored mainly in the bones. Zinc is required for bone growth and homeostasis and is also a crucial cofactor for numerous proteins that play key roles in maintaining microstructural integrity and bone remodeling. Bone marrow-derived mesenchymal stem cells (BMSCs) are multipotent progenitors found in the bone marrow stroma and can differentiate along multiple lineage pathways. In this study, we investigated the effect of zinc on the osteogenic differentiation of BMSCs. We stimulated the osteogenic differentiation of BMSCs with high phosphate and Ca-containing osteogenic medium (PiCa) in the presence or absence of zinc. We followed calcification by measuring ECM mineralization, the Ca content of the ECM, mRNA, and the protein expression of the osteo-chondrogenic transcription factor RUNX2 and SOX9 and its targets OCN and ALP. Zinc dose-dependently abolished PiCa-induced ECM mineralization and decreased the expression of RUNX2, SOX9, OCN, and ALP. Serum albumin did not alter the inhibitory effect of zinc on BMSC mineralization. Our further analysis with the zinc-chelator TPEN and ZnCl confirmed the specific inhibitory effect of free zinc ions on BMSC mineralization. Zinc inhibited phosphate uptake and PiCa-induced upregulation of the sodium-dependent phosphate cotransporters (PiT-1 and PiT-2). Zinc attenuated the PiCa-induced increase in ROS production. Taken together, these data suggest that zinc inhibits PiCa-induced BMSC calcification by regulating phosphate uptake and ROS production.
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http://dx.doi.org/10.3390/nu16234012 | DOI Listing |
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11643862 | PMC |
Acta Biomater
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Beijing Advanced Innovation Center for Materials Genome Engineering, State Key Laboratory for Advanced Metals and Materials, School of Materials Science and Engineering, University of Science and Technology Beijing, Beijing 100083, PR China; Institute of Materials Intelligent Technology, Liaoning Academy of Materials, Shenyang 110004, China. Electronic address:
Strain softening is a common issue for high-strength biodegradable Zn alloys. We developed Zn-0.6Mn-0.
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January 2025
Biomedical Engineering Institute, Chiang Mai University, Chiang Mai, Thailand.
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State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China; Department of Periodontology, School & Hospital of Stomatology, Wuhan University, Wuhan, China. Electronic address:
Periodontitis (PD) is twice as prevalent in diabetics compared to nondiabetics, and diabetes-associated PD is characterized by increased inflammation and aggravated tissue damage. Pyroptosis has recently been implicated in diabetes-associated PD; however, the underlying mechanisms remain largely unknown, resulting in a lack of effective treatments. In this study, we investigated the role of methyltransferase-like 3 (METTL3) in macrophage pyroptosis and found that it inhibits the osteogenic differentiation of osteoblasts via pyroptotic macrophages in a diabetes-associated periodontitis mouse model.
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Implant Department, Beijing Stomatological Hospital, School of Stomatology, Capital Medical University, Tiantan Xili No.4, Dongcheng District, Beijing, 100050, China. Electronic address:
As a GLP-1 receptor agonist widely used in treating type 2 diabetes, liraglutide shows potential applications in bone tissue engineering. This study investigated liraglutide's direct effects on rat bone marrow mesenchymal stem cells (BMSCs) osteogenic differentiation and its regulatory mechanism through macrophage polarization. Results showed that liraglutide significantly enhanced BMSC migration and osteogenic differentiation.
View Article and Find Full Text PDFInt J Biol Macromol
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Department of Orthopedics, Peking University Third Hospital, Beijing, China; Engineering Research Center of Bone and Joint Precision Medicine, Beijing, China. Electronic address:
The repair of diabetic bone defects is still filled with enormous challenges. Excessive reactive oxygen species (ROS) are regenerated in diabetic bone defect sites which is harmful to bone regeneration. Therefore, it's to a good strategy to scavenge the excess ROS to provide a friendly environment for diabetic bone defects repair.
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