Fig 1: BMSCs-IGF-1 resistance to hypoxia is dependent on AKT. BMSCs-NC or BMSCs-IGF-1 were treated with 0.5 µM LY294002 or an equal volume of DMSO for 24 h, and then, the cells were exposed to hypoxia for 48 h. a Cell proliferation was determined by MTS assay. b, c Cell migration was determined by Transwell assay. d Expression of p-AKT, AKT, SFRP2, ß-catenin, cyclin D1, c-myc, BAX, BCL-2, and cleaved caspase-3 were determined by Western blotting. All assays were performed in triplicate (*P < 0.05, **P < 0.01, ***P < 0.001)
Fig 2: Comparison of systemic factors using enzyme-linked immunosorbent assays (ELISA). Brain-derived nerve growth factor (BDNF) was upregulated after both AE and NMES, with the most dramatic change evident after a medium dose of NMES resulting in an almost 8-fold increase. Little change was evident in VEGF-A, with only the low AE condition showing a minor non-significant 6% increase. The low AE condition also increased IGF-1 by 33% and showed an AE dose-dependent decrease, with the medium condition being equivalent to control levels. NMES did not affect IGF-1 levels. In contrast, Klotho revealed a significant AE dose-dependent modulation of levels with a medium dose of AE doubling the amount of Klotho in the blood compared to controls. NMES also produced an increase of Klotho for the low and high condition, but not for the medium dose. (*p < 0.05; **p < 0.01).
Fig 3: Hippocampal gene expression. BDNF mRNA was upregulated after AE, but did not exhibit a dose-dependency. A significant 10% increase in hippocampal BDNF was evident after low NMES and showed a dose dependent decrease to the level of controls. VEGF-A was upregulated in all NMES conditions, but did not change after a medium and high dose of AE. A low dose actually decreased VEGF-A expression. IGF-1 was upregulated in all conditions by approx. 17%. Only the low AE condition produced a lower 5% upregulation. Klotho revealed an expression profile similar to IGF-1 (27% increase), but with a more marked increase in expression in the low AE condition (12%). (*p < 0.05; **p < 0.01).
Fig 4: The schematic diagram for anatase and rutile TiO2 NPs damage bone structure in young rats via the IGF-1/OPG/RANKL/CTSK pathway. Data from these studies. 43,44
Fig 5: BMSCs-IGF-1 protected H9C2 rat cardiomyoblast cells against hypoxia. H9C2 were co-cultured with BMSCs-NC, BMSCs-IGF-1, or control medium, and then exposed to hypoxia for 48 h. a Cell proliferation of H9C2 was determined by MTS assay. b, c Apoptosis of H9C2 was determined by Annexin-V-FITC staining. d Expression of BCL-2, BAX, and cleaved caspase-3 in H9C2 was determined by Western blotting. All assays were performed in triplicate (*P < 0.05, **P < 0.01, ***P < 0.001)
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