Manipulating calcium accumulation in blood vessels may provide a new way to treat heart disease

April 9, 2013

Hardening of the arteries, or atherosclerosis, is the primary cause of heart disease. It is caused by calcium accumulation in the blood vessels, which leads to arteries becoming narrow and stiff, obstructing blood flow and leading to heart complications. Although many risk factors for atherosclerosis have been identified, the cause is not known and there is currently no way to reverse it once it sets in. In a new study published 9th April in the open access journal PLOS Biology, researchers have characterized the cells responsible for driving this calcium build-up in vessel walls.

The process of calcium accumulation in resembles and involves maintaining a balance between bone-forming cells called osteoblasts and bone-destroying cells called osteoclasts. In the new study, Hyo-Soo Kim and colleagues characterize the origin of a population of vascular calcifying progenitor cells, and the potential of these cells to differentiate into different cell types.

"We show that vascular calcifying progenitor cells in the artery have the potential to become either osteoblasts or osteoclasts," said Dr Kim of Seoul National University. "And a certain chemical can push these cells towards becoming osteoclasts, which leads to the softening of the blood vessels."

The researchers sorted cells from the aortas of mice into two groups. Both groups originated from bone marrow and expressed a , called Sca-1, but only one group expressed another cell surface protein called PDGFRα. They found that the cells which only expressed Sca-1 could become either osteoblasts or osteoclasts, whereas the cells which expressed both Sca-1 and PDGFRα were committed to an osteoblastic lineage.

The team then treated the cells with a protein called PPARγ, which is known to promote the formation of osteoclasts and inhibit the formation of osteoblasts. When treated with PPARγ, only Sca-1 expressed cells preferentially differentiated into osteoclast-like cells. Furthermore, in vivo study demonstrated that, while bidirectional cells that were injected into mouse models of atherosclerosis increased the severity of calcium build-up in arteries, cells that were then treated with a drug activating PPARγ markedly decreased this effect and even reversed the calcification.

"These findings suggest that a subtype of calcifying progenitor cells offer a new therapeutic target for the prevention of calcification," said Dr Kim. "This opens up the possibility of new drug development to inhibit the hardening of the arteries, and thereby reduce the risk of heart disease."

Explore further: Mouse study suggests vitamin E may weaken bones

More information: Cho H-J, Cho H-J, Lee H-J, Song M-K, Seo J-Y, et al. (2013) Vascular Calcifying Progenitor Cells Possess Bidirectional Differentiation Potentials. PLoS Biol 11(4): e1001534. doi:10.1371/journal.pbio.1001534

Related Stories

Research uncovers new protein to treat damaged bones

January 10, 2013

Korean researchers believe that the 'DJ-1 protein' can be used to promote the formation of new bone tissue in patients suffering from osteoporosis by improving communication between bone making cells (osteoblasts) and blood ...

Recommended for you

Researchers find sleep gene linked to heart failure

November 30, 2015

Researchers at the Stanford University School of Medicine have identified a gene that, when working properly, appears to reduce the risk of heart failure and improve treatment outcomes, highlighting a possible target for ...

No new heart muscle cells in mice after the newborn period

November 5, 2015

A new study from Sweden's Karolinska Institutet shows that new heart muscle cells in mice are mainly formed directly after birth. After the neonatal period the number of heart muscle cells does not change, and A new study ...

1 comment

Adjust slider to filter visible comments by rank

Display comments: newest first

not rated yet Apr 10, 2013
The concentration of the PPARγ agonist, rosiglitazone (5 mg/kg/d), used in the mice study was higher than the human AUC (area under curve) of the FDA-recommended clinical daily dose.

Recent studies have shown there may be an increased risk of coronary heart disease and heart attacks with rosiglitazone.

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.