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Newly discovered gene controls levels of 'bad' cholesterol in mice

injected the virus into normal mice, where it made Pcsk9 protein inside liver cells.

With abnormally high levels of Pcsk9 in their livers, the mice developed high cholesterol. Four days after injection, the animals' LDL levels were five times the normal level, and their levels of total cholesterol in the bloodstream had doubled. (Total cholesterol measures LDL plus HDL plus another type of cholesterol.)

Maxwell suspected that the Pcsk9 protein was raising LDL levels by acting on the liver cells' LDL receptors, which snatch up LDL molecules from the blood.

To test this hypothesis, Maxwell injected the Pcsk9-carrying virus into a strain of mice that do not have LDL receptors because of a genetic defect. When Maxwell examined the special high-cholesterol mice after they had been injected with Pcsk9, she found that their cholesterol levels had not changed -- LDL levels did not increase as they had in normal mice. This suggests that Pcsk9 has no effect on cholesterol levels unless LDL receptor molecules are present.

In addition, Maxwell found that normal mice injected with the Pcsk9 lost their liver LDL receptors. This indicates that Pcsk9 directly affects LDL receptors.

"LDL receptors are the main way of getting LDL out of the blood," said Maxwell. "I think knowing that Pcsk9 modulates LDL receptors is important for understanding how LDL levels are regulated."

Maxwell and Breslow said it is unclear why Pcsk9 gene mutations cause high cholesterol in humans but this work in mice should help to figure this out.

"If the same mechanism Maxwell found in mice pertains to humans and we could inhibit Pcsk9 with drugs, this should increase the number of LDL receptors on cells and in this way lower LDL levels in the blood. This might offer another therapeutic approach to the high blood cholesterol levels that are a major risk factor for heart disease," said Breslow, a former president of the American Heart Association.
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26-Apr-2004


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