Human genes and those of other mammals are similar enough that scientists can learn a lot about the human body by studying animals. But a new study from OMRF shows that sometimes we aren’t as similar to our animal cousins as we think.
A new paper in the Journal of Experimental Medicine by OMRF scientists Rodger McEver, M.D., and Zhenghui Liu, M.D., Ph.D., shows that the regulation of a protein commonly studied for its part in blood clotting and inflammation differs greatly between mice and humans. It may offer new insights into the causes of heart attacks and strokes.
The protein, known as P-selectin, appears very similar in mice and humans. “But we found that it behaves more differently than scientists assumed, which means some of the previous research needs to be re-examined,” said McEver, who holds the Alvin Chang Chair in Cardiovascular Biology at OMRF.
When there’s an infection or tissue injury, the human body calls for the protein to help grab hold of white blood cells, which fight illness. In mice, signaling molecules encourage the body to make more of the protein. But in humans, the signaling molecules have no effect or cause the body to make less of the protein.
“That’s not to say that these signaling molecules aren’t important in humans—they are—but they don’t do what we thought they did,” he said.
McEver’s lab bred a kind of mouse that carries the human gene for the protein instead of the normal mouse gene. The OMRF scientists will continue to study the animals to better understand how the protein works in people.
This means researchers will take a new look at the role of P-selectin in atherosclerosis and other heart diseases, infections and immune responses for information about the causes and possible treatments for illnesses.
The research was done with the help of OMRF scientists Florea Lupu, Ph.D., Lijun Xia, M.D., Ph.D., Tadayuki Yago, M.D., Ph.D., and Longbiao Yao, M.D. The work was funded by a grant from the National Heart, Lung and Blood Institute.