TABLE 1.
The differences between normoxic and hypoxic MSCs.
| Cell type | Differences | Ref |
|---|---|---|
| Normoxic MSCs | - Differentiate into osteoblast most rapidly | Raheja et al. (2010b) |
| - Survival rate is Low compared to hypoxic conditions | Wang et al. (2008a), Hu et al. (2008) | |
| - Degrade phosphorylation of the Akt signaling pathway | Hill et al. (2009) | |
| - Cell proliferation rate is Low compared to hypoxic conditions | Grayson et al. (2007b) | |
| - Transcriptional activity of hypoxia inducible factor-1 (HIF-1) is ubiquitinated and degraded and reduce the angiogenesis | Hill et al. (2009) | |
| Hypoxic MSCs | - Reduce differentiate into osteoblast | Raheja et al. (2010b) |
| - Increased adipogenic and osteogenic differentiation | Basciano et al. (2011a), Valorani et al. (2012) | |
| - Enhanced skeletal muscle regeneration, improved blood flow and vascular formation | Leroux et al. (2010) | |
| - Expression of chemokine receptors CXCR4, CXCR7, and CX3CR1 was upregulated (play an important role in damaged-tissue-specific trafficking and homing of MSCs) | Hung et al. (2007a), Liu et al. (2012a), Saller et al. (2012), Tsai et al. (2012) | |
| - Increased level of glucose resulting from gluconeogenesis | Ren et al. (2006a), Martin-Rendon et al. (2007a), Hung et al. (2007b) | |
| - Overexpression of HIF-1, increase in erythropoietin receptors, and anti-apoptotic factors Bcl-2 and Bcl-XL, followed by decreased Caspase-3 levels | Wang et al. (2008a), Hu et al. (2008) | |
| - Increase phosphorylation of the Akt signaling pathway | Hill et al. (2009) | |
| - Increased cell proliferation rate | Grayson et al. (2007b), Martin-Rendon et al. (2007b) | |
| - Enhanced the migration capacity | Hung et al. (2012c) | |
| - Decreased the time necessary for the cell population to double and increase in the number of cells in the G2/S/M phase | D’Ippolito et al. (2006), Ren et al. (2006b) | |
| - Increased secretion of VEGF and (MT1-MMP), reduced levels of (MMP2) | Wu et al. (2007) | |
| - Decreased expression of TGF-β3, increased expression of FGF2 and VEGF | Potier et al. (2007) |