Endothelial cells are thought to newly emerge from the mesoderm to form the entire circulatory system. Lately, erythro-myeloid progenitors (EMPs) have been proposed to be a remarkable developmental origin for blood vessels in multiple organs, including the heart, lung, liver, and hindbrain, as shown by lineage tracing studies using a variety of genetic tools. The aim of this study was to examine the contribution of EMPs to intraembryonic endothelial cells.
Transgenic mice were chosen that expressed a tamoxifen-inducible Mer-iCre fusion protein driven by the Csf1r promoter. Genetic lineage tracing based on Csf1r-Mer-iCre-Mer showed no contribution of EMPs to brain endothelial cells identified by several markers. It was found that Kit (KIT proto-oncogene receptor tyrosine kinase) was expressed not only in EMPs but also in embryonic hindbrain endothelial cells. CD45 (protein tyrosine phosphatase receptor type C; Ptprc)+ circulating EMPs was also traced in this study, however, no CD45 lineage-derived endothelial cells were found during the development.
In conclusion, the collective data disputes against EMPs being another developmental origin of blood vessels in mice. The current results support that embryonic endothelial cells emerge only through the classical pathway of differentiation from the mesodermal-derived angioblast precursor cells.
Ref: https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.120.317442
