When Huang grew mice with a "knock out" mutation that blocked cell division among the radial glia, he expected to see abnormalities in the embryonic brain. But the major abnormality was completely unexpected: blood vessels that had already formed had collapsed.
New blood vessels in an embryo generally develop via a two-step process, first growing, and then stabilizing. "If the second step cannot be carried out, the vessels may already be formed, but the organ still cannot get its blood supply because the vessel will regress, or collapse," Huang says.
When blood vessels collapse, neurons start to die, says Huang. Some brain diseases, including Alzheimer's and hemorrhagic stroke, show a similar regression, and Huang says it's possible that the signaling mechanism that he experimentally blocked may play a role in these diseases as well.
Although any clinical treatment is years away, Huang is still basking in the thrill of basic discovery.
"We find that these progenitor and helper cells, the radial glia, regulate blood vessel development, and nobody has found that before." Huang says. "We used a mouse with alterations in genetics that regulate activity in these helper cells in the brain, and were very surprised to see that this had a drastic effect on blood vessel development. Previously it was always thought that these were two separate systems, now we know there is crosstalk between them. It's almost like a new field has opened up."
|Contact: Zhen Huang|
University of Wisconsin-Madison