Scientists suggest genetic shutdown links estrogen, heart disease

An age-related drop in estrogen may not be the only reason heart disease in women sharply increases after menopause, a new study by Johns Hopkins researchers suggests. A large-scale genetic event that quietly blocks arteries' ability to respond to estrogen may also be at work.

"Our findings could account for the perplexing results of a recent multicenter study that showed many women with existing coronary artery disease get no heart-saving benefit from hormone replacement therapy," says Wendy S. Post, M.D., who led the research team.

The new research, reported in the September edition of the journal Cardiovascular Research, centers on the fact that blood vessels in the heart are dotted with receptors for the hormone estrogen. When the scientists examined genes that direct the production of estrogen receptors (ERs), they discovered a significant difference between the ER genes from healthy heart vessels and those from vessels clogged by atherosclerosis.

In the healthy vessels, a small number of those genes -- around 4 or 5 percent -- were changed by a process called methylation. Methylation is nature's equivalent of taping over a bar code so it can't be read; small molecules attach to a gene's "on switch," a stretch of DNA called the promoter region, and shut the gene down.

But in clogged heart blood vessels, the researchers found almost three times more methylated ER genes -- around 11 percent.

"We've been looking for the link between estrogen, menopause and atherosclerosis," says Post. "Having estrogen receptor genes shut down so tissues can't respond to estrogen appears to be a significant step."

The real significance, Post says, relates to what happens in atherosclerosis. As part of vessel disease, smooth muscle cells in a blood vessel's wall tend to grow out of control -- "not unlike a tumor," says Post. "Normally, estrogen inhibits smooth muscle overgrowth." But, she

Contact: Marjorie Centofanti
Johns Hopkins Medical Institutions

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