Fibroblast growth factor-2 ameliorates tumor necrosis factor-alpha-induced osteogenic damage of human bone mesenchymal stem cells by improving oxidative phosphorylation
Autor: | Yishan Hao, Minting Wu, Jinming Wang |
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Rok vydání: | 2020 |
Předmět: |
Apoptosis
Stimulation Oxidative phosphorylation Biology Fibroblast growth factor Oxidative Phosphorylation 03 medical and health sciences Osteogenesis Humans Glycolysis MTT assay Molecular Biology Cell Proliferation 030304 developmental biology 0303 health sciences Tumor Necrosis Factor-alpha 030306 microbiology Regeneration (biology) Mesenchymal stem cell Cell Differentiation Mesenchymal Stem Cells Cell Biology Cell biology Fibroblast Growth Factor 2 Tumor necrosis factor alpha |
Zdroj: | Molecular and Cellular Probes. 52:101538 |
ISSN: | 0890-8508 |
Popis: | Tumor necrosis factor-alpha (TNF-α) has been shown to have an inhibitory effect on the osteogenic differentiation of mesenchymal stem cells. The metabolic switch from glycolysis to oxidative phosphorylation (OXPHOS) is vital for energy supply during osteogenic differentiation. However, the metabolic switch is inhibited under inflammatory stimulation. FGF2 has shown that it can improve osteogenic differentiation and promote autoimmune inflammation. In this study, we investigated whether FGF2 can ameliorate TNF-a-inhibited osteogenic damage by improving OXPHOS. Effects of TNF-α or FGF2 on the proliferation and osteogenic differentiation of hBMSCs were evaluated by MTT assay, qRT-PCR, and ALP activity tests. The function of FGF2 on the TNF-a-inhibited metabolic switch was determined by Mito Stress test. The results showed that TNF-α was able to inhibit the osteogenic differentiation and OXPHOS of hBMSCs. FGF2 has no obvious function in improving the osteogenic-related genes, but it can ameliorate the impaired osteogenesis and OCR value caused by TNF-α. These findings suggest that FGF2 can prevent the impaired osteogenic differentiation and metabolic switch of hBMSCs under inflammatory stimulation, which might enhance the regeneration capacity of hBMSCs. |
Databáze: | OpenAIRE |
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