It can be called a major step towards the use of stem cell therapies for heart disease. The researchers in the University of Bristol, found that our bodies’ ability to respond to an internal ‘mayday’ signal may hold the key to success for long-awaited regenerative medicine. Their findings also provide a practical step to advance progress in stem cell therapies.

In healthy people, reduced oxygen supply can occur in certain situations, e.g. after an injury. The affected tissues release chemical messengers that ‘call’ to a type of circulating stem cells (EPCs) for help to re-establish blood supply via the growth of new blood vessels. A group of Bristol researchers have found that kinins, for long time considered inflammatory substances, are among the messengers supporting blood vessel growth.

In this study, published in Circulation Research, Dr Kränkel and colleagues found that EPCs respond to kinins by travelling to the target tissue and invading it to assist healing. In patients with angina, EPCs cannot respond to the distress call because they lack a kinin sensor (the ‘kinin receptor’) on their surface. The oxygen-starved tissue is therefore left with reduced blood supply.In heart attack patients they saw that a proportion of the circulating EPCs were able to sense the kinin signal and respond.

Dr Kränkel, Research Associate at the Bristol Heart Institute, said:

“Our findings showed that heart attack patients possess the functional cells needed to repair blood supply to their heart, but they’re hidden amongst a muddle of others. In previous clinical stem cell trials, a mixture of different types of cells were used. We’ve used kinin like a magnet to attract and extract the most effective repair cells from the mass of different types. This enriched sample should increase the therapeutic potential, especially in heart attack patients where quick and efficient treatment is crucial for long term outcome.”

The study was funded by grants from the British Heart Foundation, European Foundation for the Study of Diabetes, Juvenile Diabetes Research Foundation and Novo Nordisk.

Source: University of Bristol