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Enzyme provides built-in protection against atherosclerosis

Date:
July 1, 2015
Source:
University of Michigan Health System
Summary:
A new study reveals enzyme CD39 is capable of clearing the atherosclerotic plaque that leads to so many heart attacks and strokes.
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Staying active, never smoking and controlling diabetes and cholesterol can prevent hardening of the arteries, but effective treatment of atherosclerosis could come down to harnessing an enzyme already built in to the blood vessels.

Atherosclerosis is the usual cause of heart attacks, strokes and peripheral vascular disease -- conditions that all together are called cardiovascular disease, the No. 1 killer in America.

In a new study published online ahead of print in the August issue of The Journal of Clinical Investigation, scientists at the University of Michigan Health System used mice to show that a human membrane-bound enzyme called CD39, which can clear the dangerous buildup of adenosine triphosphate (ATP) from the bloodstream, significantly reduces atherosclerosis in mice.

The enzyme is known for its ability to control blood clots and reduce inflammation, but the study led by Yogen Kanthi, M.D., and David Pinsky, M.D., is the first to reveal a major role of CD39 in reducing atherosclerosis.

"Better lifestyles and improved treatments have slowed the rates of death from atherosclerosis, but if CD39 proves to be as critical a factor in humans as in mice, it would be a major step forward in understanding heart disease," says senior study author David Pinsky, M.D., cardiologist and director of the University of Michigan Frankel Cardiovascular Center.

Atherosclerosis is a progressive process that puts blood flow at risk. It begins with damage -- caused by high cholesterol, high blood pressure or smoking -- to the thin layer of cells lining the blood vessels.

The damage can lead to an accumulation of cholesterol, cells and debris called plaque that not only puts the heart at risk, but also raises the risk of stroke, peripheral artery disease and other health problems.

The benefit of CD39, according to the lab study, is in its ability to control plaque formation.

"We found that when we reduced CD39 expression, the size of atherosclerotic plaque doubled," says lead study author Yogen Kanthi, M.D., cardiologist and vascular medicine specialist at the U-M Frankel Cardiovascular Center.

The team of investigators from the U-M and Emory University made the discovery that CD39, which lines blood vessels, is regulated by blood flow patterns in mice and in human cells. More research is needed before any potential treatments might become available.

"Plaque predictably occurs in branch points in arteries, where blood flow is turbulent and not smooth," Kanthi says. "These same areas of turbulent blood flow are ones with the least amount of CD39 lining the artery. The study reveals a key role of CD39 in preventing atherosclerosis and opens new avenues for targeted treatment possibilities in coronary and peripheral artery diseases."


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Materials provided by University of Michigan Health System. Note: Content may be edited for style and length.


Journal Reference:

  1. Yogendra Kanthi, Matthew C. Hyman, Hui Liao, Amy E. Baek, Scott H. Visovatti, Nadia R. Sutton, Sascha N. Goonewardena, Mithun K. Neral, Hanjoong Jo, David J. Pinsky. Flow-dependent expression of ectonucleotide tri(di)phosphohydrolase-1 and suppression of atherosclerosis. Journal of Clinical Investigation, 2015; DOI: 10.1172/JCI79514

Cite This Page:

University of Michigan Health System. "Enzyme provides built-in protection against atherosclerosis." ScienceDaily. ScienceDaily, 1 July 2015. <www.sciencedaily.com/releases/2015/07/150701084241.htm>.
University of Michigan Health System. (2015, July 1). Enzyme provides built-in protection against atherosclerosis. ScienceDaily. Retrieved May 23, 2017 from www.sciencedaily.com/releases/2015/07/150701084241.htm
University of Michigan Health System. "Enzyme provides built-in protection against atherosclerosis." ScienceDaily. www.sciencedaily.com/releases/2015/07/150701084241.htm (accessed May 23, 2017).

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