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Blocking the nerve receptor EP1 in mouse models reduces brain damage caused by stroke

Researchers at Johns Hopkins have discovered how to block a molecular switch that triggers brain damage caused by the lack of oxygen during a stroke. The Hopkins study, conducted on mice, is believed to be the first to demonstrate that a protein on the surface of nerve cells called the EP1 receptor is the switch, and that a specific compound, known as ONO-8713, turns it off.

The finding holds promise for the development of effective alternatives to anti-inflammatory drugs called COX inhibitors, which have potentially lethal side effects that limit their use, says Sylvain Doré, Ph.D., an associate professor in the departments of Anesthesiology and Critical Care Medicine and Neuroscience at The Johns Hopkins University School of Medicine. Doré is senior author of the paper, published in the January issue of Toxicological Sciences. "Our work has shifted the focus from drugs that inhibit COX-2 to drugs that block the EP1 receptor," Doré said.

Receptors are protein-docking sites on cells into which "signaling" molecules such as nerve chemicals or hormones insert themselves. This binding activates the receptor, which transfers the signal into the cell to produce a specific response.

COX inhibitors block the ability of the enzyme cyclooxygenase-2 (COX-2) to make prostaglandin E2 (PGE2), a hormonelike substance long linked to inflammation and other effects. The Hopkins study results suggest that PGE2 causes brain damage following stroke by binding to the EP1 receptor on nerve cells. Therefore, blocking PGE2 activity directly rather than inhibiting COX-2 could reduce brain damage in individuals who have a stroke while avoiding the side effects of COX-2 inhibitors, the Hopkins investigators say.

Previous work by others had shown that certain events, such as cerebral ischemia (stroke) and seizures, that interrupt oxygen flow to the brain also cause excessive activation of so-called NMDA receptors by the nerve chemical glutamate. Other work had
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Source:Johns Hopkins Medical Institutions


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