Table 1.
Group | Identification markers | Organ source | Hierarchy | Pathological implications |
---|---|---|---|---|
Fang et al. | CD31 + CD105 + Sca1 + CD117 + Lin- | Lungs, liver, kidneys | No | Neovascularisation in B16 melanoma |
Naito et al. | CD31 + CD45-Vecad + SP | Lungs, liver, hindlimb muscle, heart | No | Vascular regeneration following ischaemic injury |
Yu et al. | CD31 + CD105 + Sca1 + Lin-Procr+ | Mammary glands, Retina | No | Tumour vascularisation and fibrotic diseases |
Wakabayashi et al. | CD31 + Vecad + CD45-CD200 + CD157+ | Lung, hindlimb muscle, heart, retina, skin, brain, aorta | Yes | Peripheral vessel regeneration and rescue of haemophilia |
Patel et al. | Vecad + CD34 + Lin-CD31lo VEGFR2lo | Aorta, lung, skin | Yes | Neovascularisation in tumour, wound healing |
Various groups have established phenotypic signatures for murine EPCs in hopes to mimic and gather a greater understanding of human endothelial colony-forming cells (ECFCs). Inclusion and exclusion of markers have been used to define murine EPCs in a suite of organ beds, some of which govern a maturation hierarchy of endothelial differentiation. Understanding how these EPCs function in homeostasis as well as pathological contexts offers vast potential for vascular implicated diseases
SP side population, Vecad vascular endothelial cadherin, Lin lineage cocktail