Table 1.
Effects of chemical factors on bone marrow-derived mesenchymal stem cell (BMSC) migration
| Chemical Factor | Concentration | Cell Migration | Outcomes | References |
|---|---|---|---|---|
| Stromal derived factor-1(SDF-1) | 50 ng/mL, 100 ng/mL | ↑ | SDF-1 increased BMSC recruitment to injured liver and promoted the repair of injured liver. | [16] |
| SDF-1 | 100 ng/mL | ↑ | SDF-1 increased BMSCs with CXCR4 expression and promoted the repair of traumatic brain injury. | [17] |
| SDF-1 | 10 ng/mL | ↑ | SDF-1 increased stem cell recruitment, and the pretreatment of stem cells (Wharton’s jelly-derived mesenchymal stem cells (WJ-MSCs), embryonic stem cells (ESCs)) enhanced skeletal muscle regeneration. | [18] |
| Osteopontin (OPN) | 1 μg/mL | ↑ | Increased integrin β1 expression in BMSCs and promoted BMSC migration through the ligation to integrin β1. | [19] |
| OPN | 10 μg/mL, 20 μg/mL | ↑ | Increased mesenchymal stem cell (MSC) migration in a dose-dependent manner. | [20] |
| OPN | 1 μg/mL | ↑ | OPN reduced the number of organized actin cytoskeletons through the FAK and ERK pathways to increase BMSC migration. | [21] |
| OPN | 1 μg/mL | ↑ | Reduced the number of organized actin cytoskeletons through the FAK and ERK pathways to increase BMSC migration. | [22] |
| OPN | 1 μg/mL | ↑ | Cytoskeletal control of nuclear morphology and stiffness through the SUN1 proteins plays an important role in OPN-promoted BMSC migration. | [23] |
| OPN | 1 μg/mL | ↑ | Chromatin organization was altered by the application of OPN via the ERK1/2 signaling pathway, which also contributed to BMSC migration. | [24] |
| Basic fibroblast growth factor (bFGF) | 200 ng/mL | ↑ | Augmented the engraftment and differentiation capacity of transplanted BMSCs, recovering cardiac function. | [25] |
| bFGF | 1 ng/mL up to 400 ng/mL | ↓↑ | Low concentrations led to an attraction of BMSCs, whereas higher concentrations resulted in repulsion. | [26] |
| Vascular endothelial growth factor (VEGF)-A | 10 ng/mL | ↑ | Increased BMSC migration and proliferation. | [27] |
| Hepatocyte growth factor (HGF) | 20 ng/mL | ↑ | Increased BMSC migration via PI3K pathways. | [28] |
| Insulin-like growth factor (IGF)-1 | 10 ng/mL | ↑ | Increased BMSC migratory responses via CXCR4 chemokine receptor signaling, which is PI3/Akt-dependent. | [29] |
| IGF-1 | 20 ng/mL | ↑ | Preconditioning of BMSCs with IGF-1 before infusion improved cell migration capacity and restored normal renal function after acute kidney injury. | [30] |
| Platelet-derived growth factor (PDGF) | 50 ng/mL | ↑ | Increased BMSC migration significantly. | [31] |
| PDGF-B | 40 ng/mL | ↑ | Increased recruitment/migration and differentiation of BMSCs. | [32] |
| Transforming growth factor (TGF)-β 1 | 100 pM | ↑ | Promoted the homing of BMSCs in myocardial ischemia/reperfusion injury and improved myocardial function. | [9] |
| TGF-β1 | 5 ng/mL | ↑ | Improved BMSC recruitment and wound closure in a syngeneic murine wound model. | [33] |
| TGF-β | 1 ng/mL~100 ng/mL | ↑ | Activated noncanonical signaling molecules, such as Akt, ERK1/2, FAK, and p38, via TGF-β type I receptor to increase stem cell (BMSCs, BM-MSC-like ST2 cells) migration. | [34] |