Such clots cause 80 percent of the 15 million strokes that occur each year worldwide. Five million people die, and 5 million more are permanently disabled, by strokes each year, according to the World Health Organization.
"Our findings may have immediate clinical relevance, and could be applied to find new treatments that will benefit stroke patients," says senior author Daniel Lawrence, Ph.D., professor of cardiovascular medicine in the U-M Medical School and member of the U-M Cardiovascular Center. "By better understanding how the brain regulates the permeability of the blood-brain barrier, and how tPA acts upon that system, we hope to reduce the risks and increase the time window for stroke treatment."
Ulf Eriksson, Ph.D., the leader of the team at the Ludwig Institute for Cancer Research Stockholm Branch at Karolinska Institutet, comments, "Our research group identified the growth factor PDGF-CC ten years ago and we are now very excited having unraveled a mechanism in the brain involving this factor, which potentially will be a revolution in the treatment of stroke. Together with our clinical colleagues at the Karolinska University Hospital in Stockholm we are now rapidly continuing to explore this exciting possibility in clinical trials involving stroke patients."
Eriksson and Lawrence collaborated with a number of colleagues -- including lead author Enming Joe Su, Ph.D. of U-M and teams at Karolinska Institutet, the University of Maryland and Emory University -- to perform the study.
Some of the mice in the study lacked the natural tPA that the body makes on its own. Some of the mice underwent a procedure that simulated the effects of a clot-based, or ischemic, stroke.
The researchers first demonstrated in non-stroke mice that tPA and
PDGF-CC appeared to act
|SOURCE University of Michigan Health System|
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