Duke study: Aging uses up body’s ‘repair parts’

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By Jim Shamp : The Herald-Sun jshamp@heraldsun.com Nov 19, 2002 : 10:25 pm ET

DURHAM -- Hardening of the arteries -- atherosclerosis -- might be a disease of old age because people use up their limited supply of "repair parts" during their devil-may-care youth, according to Duke University Medical Center researchers.

The new view, aired by a fourth-year Duke medical student Tuesday, is based on research in mice specially bred to develop high cholesterol and clogged arteries.

The student, Frederick Rauscher, said his research has shown that a certain strain of stem cells in bone marrow, called progenitor cells, are continually called out of the marrow to repair sites of normal recurring vascular injury or inflammation.

That injury may be caused by a variety of assaults, including infections, smoking, high cholesterol, high blood pressure and diabetes.

Stem cells are immature cells that have the potential to take on a variety of roles in maturity.

Somewhere around middle age, according to Rauscher, the demand for active repair cells starts to outstrip the supply. That opens the door to a cascade of damage along arterial walls, often resulting in blockages creating heart attacks or strokes.

Rauscher and his mentor, Duke cardiology chief Pascal Goldschmidt, see the discovery pointing to possible therapies for avoiding or treating the plaque buildup of atherosclerosis. Those might include medicines that could "wake up" existing but inactive progenitor cells in the patient’s own marrow, or injecting stem cells from donors -- possibly even cells from umbilical blood.

What’s more, said Rauscher, the problem of used-up progenitor cells might help explain other degenerative disorders normally associated with aging, such as arthritis and even Alzheimer’s disease.

"People with severe arthritis also have a big increased risk for atherosclerosis as well," said Rauscher. "It could be that the constant process of repairing joints is consuming cells from bone marrow that aren’t available later for repairing arteries.

"We began by asking the question, ‘Why is aging required for most atherosclerosis?’" Rauscher told The Herald-Sun in a phone interview Tuesday before making his presentation at the 75th annual scientific session of the American Heart Association in Chicago.

Rauscher was one of five finalists from around the world who were invited to present their research findings at the heart association meeting, competing for the coveted Louis N. and Arnold M. Katz Basic Research Prize for Young Investigators. The award program, established in 1969, now includes a prize for basic science and another for clinical studies.

He and several Duke colleagues injected progenitor cells from normal mice into the atherosclerosis-prone mice multiple times over 14 weeks. At the end of the period, the injected mice were compared with a control group that didn’t get the progenitor cells.

Though there was no difference in cholesterol levels between the mouse groups, said Rauscher, those receiving the cell injections had a 69 percent decrease in plaque buildup in their aortas, the main arteries of the heart. The plaque, identified by special stains, was also 42 percent less prevalent at the aortic root, where the aorta emerges from the main heart muscle, said Rauscher.

What’s more, he said, close examination showed the injected cells went where they were needed most, and transformed themselves into necessary cell types to perform various functions. Some became "patches" lining the artery; others turned into smooth muscle cells deeper in the artery wall to help propel blood through the artery.

"We also tried injecting cells from old mice into other old mice," said Rauscher, "and they were much, much less effective -- only a little better than nothing."

"Of course, the human organism is not designed to live 200 years," said Goldschmidt. "But as you look at the brain and the heart, you could easily say it’s genetically designed to maintain full human characteristics for 100 years, with these kinds of re-adaptations for today’s environment."

-- Anonymous, November 20, 2002


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