Table 1.
Genetic studies illustrating functions of endothelial factors in bone are summarised below.
| Factors | Modification | Functions | Reference(s) |
|---|---|---|---|
| Cxcr4 | EC-specific deletion (induced) | Increased vascular permeability HSPC egress | [35] |
| Cxcl12 | EC-specific deletion (constitutive) | Decreased HSC frequency | [69, 70] |
| Dll1 | EC-specific deletion (induced) | Monocyte development | [90] |
| Dll4 | EC-specific deletion (induced) | Regulates type H vessels Coupling of angiogenesis and osteogenesis haematopoiesis |
[10, 34] |
| Fbw7 | EC-specific deletion (induced) | Reactivating type H vessels in aged bones induce arterioles formation increase PDGFRb+, alpha-SMA+ mesenchymal cells increase HSC frequency | [10, 29, 34] |
| Fgfr1/2 | EC-specific deletion (induced) | Impaired vascular integrity reduced HSPCs and MSPCs | [35] |
| Gp130 | EC-specific deletion (constitutive) | Hypocellular marrow, marrow dysfunction, and splenomegaly | [78] |
| Hif1a Vhl |
EC-specific deletion (induced) | Regulates type H vessels Coupling of angiogenesis and osteogenesis |
[8] |
| Pdgfb | EC-specific overexpression (induced) | Increased PDGFRb+, alpha-SMA+ mesenchymal cells | [34] |
| Pecam1 | Global deletion | No substantial change in blood vessels | [29] |
| Scf | EC-specific deletion (constitutive) | Decreased HSC frequency | [81] |
| Sele | Global deletion | Promotes HSC quiescence and resistant to irradiation | [80] |