Table 1.
Chemokines of MSCs.
| Factors | Main characters | Reference |
|---|---|---|
| TGF-β | (1) TGF-β can be released by the damaged vessel cells and lesioned artery and involved in vascular regeneration and VC (2) TGF-β couples bone resorption with formation by inducing MSC migration and participates in bone and cartilage metabolism. Subchondral bone MSCs activated by TGF-β seem to initiate osteoarthritis (3) TGF-β promotes homing of BM-MSC in a tissue lesion, for example, renal ischemia-reperfusion injury (4) TGF-β may regulate the SDF-1/CXCR4 axis and MCP-1 to induce MSC homing |
[30–32, 36, 82–87] |
|
| ||
| PDGF-BB | (1) PDGF has the highest effect among other cytokines (SDF-1a, CXCL16, MIP, etc.), and PDGF-BB is the most strong one among PDGF isoforms in vitro (2) PDGF-BB has been proven to be involved in myocardial and lung functional tissue regeneration, angiogenesis, and VC by recruiting MSCs (3) PDGF-BB has been applied for bone regeneration and proven to recruit MSCs to the scaffolds |
[13, 33, 82, 88–92] |
|
| ||
| PDGF-AA | (1) PDGF-AA's chemotaxis effect is lower than that of PDGF-BB, but stronger in recruiting osteogenic differentiated progenitor cells (2) PDGF-AA can promote MSC proliferation and differentiation (3) The effect of PDGF-AA can be blocked by TGF-β |
[82, 93–95] |
|
| ||
| SDF-1 | (1) SDF-1 can be released by the endothelium and ischemic myocardium in myocardial infarction, inflammatory cardiomyopathy, and vascular injury. This cytokine also correlated with the severity of calcification (2) In inflammatory bone destruction, SDF-1 was found to be upregulated, which could possibly enhance fracture healing in osteoporotic patients by recruiting MSCs. And it also improves the vascularization of bone (3) SDF-1 promotes MSCs to repair liver injury, expanded skin, and even cancer (4) Serum SDF-1 can be increased by hypoxemia |
[34, 35, 37, 88, 96–104] |
|
| ||
| BMP2/4/7 | It has only been proven in vitro | [82, 89] |
|
| ||
| FGF | In vivo researches of FGF chemotaxis mainly focus on pulmonary fibrosis | [82, 88, 105, 106] |
|
| ||
| VEGF | (1) Chemotactic activity of VEGF has been proven in vitro. And VEGF can be released by multiple myeloma and glioma cells to improve vascularization (2) VEGF plays a role in bone regeneration (3) PDGFR-α is required |
[82, 89, 107–110] |
|
| ||
| G-CSF | (1) In vivo chemotactic activity of G-CSF is controversial (2) It may work via CXCR4/SDF-1 |
[100, 111–113] |
|
| ||
| TNF-α/IL-1β/IL-6 | These cytokines are associated with inflammation and work through the NF-κb pathway. And several researches show that they inhibit instead of promoting migration | [88, 114–118] |
|
| ||
| IGF-1 | Chemotactic activity of IGF-1 is not so assuring. Pretreatment seems more reliable | [89, 119–122] |
|
| ||
| PTH | PTH can improve osteoporosis in mice and men and spine injuries | [39, 123] |
The table shows chemokines of MSCs with a brief introduction of their characters. TGF: transforming growth factor; PDGF: platelet-derived growth factor; SDF: stromal cell-derived factor; BMP: bone morphogenetic protein; FGF: fibroblast growth factor; VEGF: vascular endothelial growth factor; G-CSF: granulocyte colony-stimulating factor; TNF: tumor necrosis factor; IL: interleukin; IGF: insulin-like growth factor; PTH: parathyroid hormone.