Blood Vessel Growth in the Brain Relies on a Protein Found in Tumor Blood Vessels

In a recent study published in the journal Development Cell, researchers from the Howard Hughes Medical Institute and Johns Hopkins University discovered several genes that are more active in tumor-associated blood vessels compared to normal blood vessels. The new research reveals the normal function of one of those genes, suggesting the potential for new anticancer drug therapies. The research originally began in 2000, and researchers compared gene activity in normal blood vessels to those infiltrating colorectal tumors. Among other differences were nine genes that were highly active in the tumor-associated blood vessels, which researchers named tumor endothelial marker (TEM) one through nine. Over the next decade, further experiments revealed clues regarding the function of individual TEMs. By 2010, it was known that mice missing TEM5, also known as GPR124, have defective blood vessel growth in the brain and spinal cord. The mice also showed defective formation of the blood-brain barrier. During this study, researchers noticed that blood vessel defects in mice missing TEM5 looked similar to the defects found in mice that were missing two members of the “Wnt” family of signaling proteins used for communication between cells. To test whether TEM5 uses the “Wnt” signaling system in blood vessels, researchers artificially activated this system specifically in blood vessels in mice lacking TEM5. The blood vessel defects disappeared, confirming the relationship between TEM5 and “Wnt.” To read more about this study, click here.