Discovery changes ideas about damage from strokes

In experiments in the laboratory and with mice, the Johns Hopkins researchers found that the chemical prostaglandin-E2 protects brain cells from damage. The finding was completely unexpected, the researchers say, because prostaglandin-E2 causes damage in other tissues and is made by an enzyme, COX-2, known to wreak havoc in the brain after injury. The findings appear in the Jan. 7 issue of the Journal of Neuroscience.

"It's kind of paradoxical, that the product of an enzyme that causes damage is itself beneficial," says Katrin Andreasson, M.D., an assistant professor of neurology and of neuroscience. "It's possible that future treatments for stroke might use drugs to block COX-2 and enhance the effects of prostaglandin-E2, providing sort of a double whammy of protection.

"Prostaglandins have not previously been implicated in reducing damage from stroke, so our finding provides a completely new strategy for tackling and understanding the condition," she adds.

In experiments with individual brain cells and with brain slices from mice, the researchers discovered that prostaglandin-E2 (PGE2), one of many related molecules created by COX-2, protects brain cells traumatized by over-stimulation or by insufficient oxygen. Furthermore, in genetically engineered mice lacking one of the receptors, or docking points, for this prostaglandin, stroke damage was much greater than in normal mice, the researchers report.

"Together, these results provide very strong evidence that PGE-2 is indeed protective in the brain even though it may not be elsewhere in the body," says Andreasson, who obtained the genetically engineered mice from Richard Breyer at Vanderbilt University School of Medicine.

After their surprising discovery, the research team searched for why PGE2 is a "good guy" in the brain. Their experiments showed that stimulation of PGE2's receptor increases production of a molecule called cyclic-AMP, which is known to he

Contact: Joanna Downer
Johns Hopkins Medical Institutions

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