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New Genetic Answers to Help Unclog Arteries

How is it that your best friend can eat fatty hamburgers and fries every day without developing clogged arteries, and you eat a low-fat diet and still have to take cholesterol medication? The answer may be all in your genes.

A new study shows that in animals bred to be susceptible to
atherosclerosis, cells in their artery walls promote the development of the
disease when exposed to LDL (the "bad") cholesterol. Dr. Weibin Shi and
colleagues at the University of California, Los Angeles, report their results in the July
4, 2000, Circulation. However, those same cells in animals bred to resist
the disease may secrete protective proteins in their artery cells.

"It's the first evidence that there are genetic factors that affect
atherosclerosis acting at the level of the vessel wall," coauthor Dr.
Aldons J.Lusis told HeartInfo/Mediconsult. The likelihood of finding a drug
that would target the problem is very good, he added. "Now we need to find
the genes involved."

In mice and humans, a high fat diet increases blood levels of LDL cholesterol and increases the risk of atherosclerosis.

In previous studies, researcher have pinpointed a couple of
genetically determined characteristics that increase a person's risk of
developing atherosclerosis, including blood pressure and the concentration
in the blood of lipoproteins or homocysteine, an amino acid. But those
characteristics can't explain the big differences in individuals'
likelihood of developing clogged arteries, unrelated to their diets.

So Dr. Shi and colleagues investigated the role of oxidized LDL. Oxidized LDL causes the cells of the endothelium to produce proteins that contribute to atherosclerosis.

They found that in certain animals it triggers endothelial cells (those lining arteries) to
stimulate several proteins that promote atherosclerosis. The proteins are
monocyte chemotactic protein-1 (MCP-1), macrophage-colony-stimulating
factor (M-CSF), and vascular cell adhesion molecule-1.

The researchers took endothelial cells from the aorta of mice bred
to be susceptible to atherosclerosis and those bred to resist it. Then
they exposed the cells to oxidized LDL, and monitored the response of
MCP-1; M-CSF; and heme oxygenase-1 (HO-1), an anti-oxidant protein that is
induced under stressful conditions and likely inhibits atherosclerosis; along with other proteins not related to inflammation or atherosclerosis.

The endothelial cells from the susceptible mice "exhibited
dramatic induction of MCP-1, M-CSF, and HO-1, whereas [the cells] from the
resistant strain showed little or no induction," the team writes. The cells
from the two strains responded similarly to lipopolysaccharide, a bacterial
inducer of inflammation that was used as a control.

In previous studies, the UCLA researchers showed that a high-fat
diet caused greater expression of MCP-1, M-CSF, and HO-1 in the liver of
mice that are susceptible to atherosclerosis than in mice resistant to it.

However, researchers don't know why susceptible mice tend to
accumulate more oxidized lipids and to be more responsive to them compared
with resistant mice, the team writes.

The study suggests a new, previously unknown factor that contributes to atherosclerosis, and may help researchers develop new tests for susceptibility, and for new treatment methods.