Printer Friendly

Lipoprotein link to heart disease revealed.

High concentrations of the cholesterol carrier lipoprotein(a) in the blood are a known risk factor for heart disease. Indeed, cardiologists estimate that Lp(a) a close cousin1 of low-density lipoprotein, itself a heart threat - may be responsible for up to 25 percent of heart attacks that strike relatively early in life. The trouble is, scientists don't understand the mechanism underlying this molecule's role in the drama of heart disease.

Now, an international scientific team suggests that elevated concentrations of Lp(a) in the bloodstream may cause smooth muscle cells within the artery wall to proliferate. As a cholesterol carrier, Lp(a) also deposits cholesterol and other fatty debris on the vessel's inner wall. The thickening of the blood vessel that results is a hallmark of atherosclerosis.

Biochemist David J. Grainger of the University of Cambridge in England and molecular biologist Richard M. Lawn at the Stanford University School of Medicine grew smooth muscle cells taken from healthy human arteries in laboratory dishes. When the team exposed those cultured cells to Lp(a), the cells began to divide more rapidly than usual. The researchers report their findings in the June 11 SCIENCE.

The new study suggests that Lp(a) interferes with a natural growth-restraining system that operates in human arteries. The group showed that Lp(a) inhibited the activation o! an antiproliferative substance called transforming growth factor-[beta]. Without enough of this activated factor, smooth muscle cells continue their division unchecked, an insidious process that could lead to clogged arteries, Lawn says.

People with high concentrations of Lp(a) in their blood may suffer the double whammy of.too much arterial muscle cell proliferation plus large deposits of cholesterol inside their artery walls. Such a mechanism may explain the elevated risk of heart attack for such people, Lawn adds.

However, both Lawn and Grainger warn that their study only looked at this cholesterol carrier's impact on smooth muscle cells grown in laboratory dishes. The team has yet to determine whether such proliferation takes place in humans.

If it does, cardiologists may one day be able to stave off atherosclerosis in people who produce too much Lp(a), says Grainger. One approach would be to use drugs that block the excess proliferation of smooth arterial muscle cells, he speculates.
COPYRIGHT 1993 Science Service, Inc.
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 1993, Gale Group. All rights reserved. Gale Group is a Thomson Corporation Company.

Article Details
Printer friendly Cite/link Email Feedback
Title Annotation:lipoprotein A may cause proliferation of smooth muscle cells within artery walls
Author:Fackelmann, Kathy A.
Publication:Science News
Article Type:Brief Article
Date:Jun 12, 1993
Previous Article:Nearby galaxy sheds light on dark matter.
Next Article:Rippling the surface of an electron sea.

Related Articles
Anatomy of atherosclerosis; in hardening of the arteries, the body's attempt to heal itself causes problems.
Smoking: clues to its heart effects.
How monounsaturates may save arteries.
Finally, proof of 'good' cholesterol's perks.
Oxidation diminishes HDL's 'goodness.' (high-density lipoproteins, the 'good' lipoproteins)
Herpes and heart disease: could viruses encourage coronary clogging?
Harbinger of a heat attack: does a protein in the blood foretell heart trouble?
Potential infectious etiologies of atherosclerosis: a multifactorial perspective. (Synopses).
Can angiotensin-converting enzyme inhibitors reverse atherosclerosis? (Review Article).
Heart-protective effect is independent of antioxidants.

Terms of use | Copyright © 2017 Farlex, Inc. | Feedback | For webmasters