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Prostaglandin receptor key to atherosclerosis development
Date:12/15/2008

The researchers found that the mice with macrophages lacking the EP4 receptor had a significant reduction in atherosclerosis compared to mice with the EP4 receptor. They also observed an increase in macrophage programmed cell death (apoptosis) in the atherosclerotic lesions of mice with EP4-deficient cells.

The team examined EP4 receptor signaling pathways and discovered that two pathways known to be involved in macrophage cell survival (PI3K/Akt and NF-kappaB pathways) had lower activity in the EP4-deficient mice, suggesting a mechanism for the increase in macrophage cell death.

"Our studies clearly show that prostaglandin-E2 plays an important role in atherosclerosis and in macrophage survival," Linton said. "Prostacyclin and thromboxane aren't the whole story."

The findings suggest the potential for modulating the development of atherosclerosis with inhibitors of prostaglandin-E2 synthesis, which are already being studied, and also by manipulating the EP receptors or their signaling pathways, Linton said.

The link between macrophage apoptosis and lesion development remains unclear, he said.

There have been some reports that increased macrophage apoptosis in early lesions reduces the lesion area, Linton said. Other studies have suggested that macrophage apoptosis creates a pro-inflammatory environment that promotes the development of more complex lesions. Still other reports speculate that macrophage cell death promotes plaque rupture, causing heart attacks and strokes.

If the latter is true, Linton said, the current studies could offer a mechanistic explanation for how the drug Vioxx increased heart attacks in patients. Vioxx, a selective inhibitor of the enzyme cyclooxygenase-2 (COX-2), was withdrawn from the market because of concern about an apparent increase in cardiovascular risk.

The current findings suggest that because COX-2 inhibition would reduce prostaglandin-E2 levels (COX enzymes perfor
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Contact: Kathy Whitney
kathy.f.whitney@vanderbilt.edu
615-322-4747
Vanderbilt University Medical Center
Source:Eurekalert

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