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(Circulation. 2003;108:e9006.)
© 2003 American Heart Association, Inc.

Cardiovascular News

Ruth SoRelle, MPH

Circulation Newswriter

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Aging of Progenitor Cells Contributes to Atherosclerosis

As bone marrow–derived epithelial progenitor cells that usually repair and give new life to aging arteries themselves become old, they are less likely to perform their tasks. This contributes to the progression of atherosclerosis, said researchers from Duke University School of Medicine in Durham, NC, in a report in this week’s issue of the journal Circulation (Circulation. 2003;108:457–463).

In the study led by Frederick M. Rauscher, MD, of Duke, mice treated with bone marrow–derived progenitor cells taken from mice that lacked the apolipoprotein E (ApoE) gene prevented progression of atherosclerosis in mice that also lacked the ApoE gene—even though the treated mice had persistent high cholesterol. When such mice were treated with bone marrow–derived progenitor cells from older mice that lacked the gene, the treatment was much less effective, the researchers reported. They found that cells with the potential of being vascular progenitors are less frequent in the bone marrow of aging mice that lack the ApoE gene. However, they said, the cells from the donor mice engraft in the areas at risk for atherosclerotic injury.

The researchers wrote: "In this mouse model of atherosclerosis, we have established that there is an atheroprotective property of the BM [bone marrow] that is ‘exhausted’ with aging and prolonged exposure to risk factors. Several findings indicate that this exhaustion likely involves progenitor cell–mediated vascular repair . . . Taken together, these results support a novel model of atherosclerosis in which deficient vascular repair, secondary to obsolescence of BM cells, is a . . . [Full Text of this Article]