11 June 2012
ByAppeared in BioNews 660
A previously unidentified type of stem cell, usually dormant in blood vessels, is at the heart of vascular disease, according to researchers.
Before this discovery, smooth muscle cells in the walls of blood vessels were blamed for the narrowing of arteries, but it may be that this was a case of mistaken identity.
Heart attacks and strokes are caused by clumps of cells building up in blood vessels, causing them to narrow. This alone restricts the blood flow, but if a lump breaks off as a clot it can move elsewhere and completely block other vessels.
Due to their appearance – the clumps of cells look like smooth muscle cells – it was thought that the build-up was triggered by an injury to the blood vessel that caused the mature smooth muscle cells to regress to an earlier developmental stage that allowed them to proliferate.
However, there was never any evidence this happened, and now a group of researchers from the University of California, Berkeley, has identified another cell type that may be the culprit. These cells, named multipotent vascular stem cells, can turn into various kinds of cells, including smooth muscle. They are present in such low numbers in healthy arteries that they haven't been noticed before.
'These stem cells are probably less than five percent of the cells in the blood vessel when they're dormant', lead researcher Professor Song Li said to the San Francisco Chronicle. 'We call them sleeping beauty or sleeping evil cells, because they don't do anything when they're dormant. The stem cells stay quiescent for decades before they start to grow and they make the blood vessels harden'.
The team found that these cells were activated when blood vessel walls were damaged, something that is thought to occur when they are damaged by low-density lipoproteins, also known as 'bad cholesterol'.
Around 150,000 people in Britain a year have a stroke; 90,000 have heart attacks, of these around a third die as a result. Professor Li claims the work, published in Nature Communications, should 'revolutionise therapies for vascular diseases'.
'Targeting the vascular stem cells rather than the existing smooth muscle in the vessel wall might be much more effective in treating vascular disease', explains co-author Dr Deepak Srivastava. 'Maybe the reason we've met with limited success in treating heart disease is because we've been going after the wrong target'.
However, they note that their results will need to be reproduced by others, and in human tissues, in order to replace the prevailing theories about how blood vessels become blocked.