The cells responsible for creating calcium build-up in vessel walls – resulting in heart disease – have now been identified in a new study published in PLOS Biology.

Atherosclerosis – or hardening of the arteries – is the main cause of heart disease. It occurs because of calcium build-up in the blood vessels – resulting in hard and narrow arteries. This then leads to problems such as blood flow obstruction and heart issues.

Several factors have been known to contribute to the risk of atherosclerosis, however, the cause is not yet known and as of now there is no way to change it once it occurs.

The risk factors for atherosclerosis include:

A study published last year in Nature Immunology suggests that atherosclerosis is caused by macrophages – white blood cells that build up in the arteries.

The system of calcium build-up in blood vessels is similar to bone formation and consists of maintaining a balance between bone-producing cells called osteoblasts and bone-eliminating cells called osteoclasts.

In the current study, Hyo-Soo Kim and co-workers categorized the starting point of a population of vascular calcifying progenitor cells, and their likelihood of differentiating into different kinds of cells.

Dr Kim, of Seoul National University, explained:

“We show that vascular calcifying progenitor cells in the artery have the potential to become either osteoblasts or osteoclasts. And a certain chemical can push these cells towards becoming osteoclasts, which leads to the softening of the blood vessels.”

The investigators organized cells from the aortas of mice into two groups. Both groups came from bone marrow and expressed a cell surface protein known as Sca-1. However just one group expressed an additional surface protein called PDGFRa.

They found that the cells which just expressed Sca-1 could develop into osteoclasts or osteoblasts, while the cells that expressed Sca-1 and PDGFRa were assigned to osteoblastic lineage.

The researchers treated the cells with a protein known as PPARy – used to aid in the production of osteoclasts and block the production of osteoblasts. When treated with PPARy, only Sca-1 expressed cells differentiated into osteoclast-like cells.

Also, the study showed while bidirectional cells that were administered into mouse models of atherosclerosis raised the severity of calcium build-up in arteries, cells that were treated with a drug triggering PPARy significantly decreased this effect and notably reversed the calcification.

Dr. Kim concludes:

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

Written by Kelly Fitzgerald