Cells in the outermost layer of the heart can be guided by a specific protein to move deeper inside and help to repair a failing adult heart. Research published today by Nature, reveals how thymosin ?4, a protein already known for its ability to reduce muscle cell loss after heart attack, can instruct the heart to heal itself.
The potential repair cells are known as progenitors. They are similar to stem cells, in that they are not yet specialised into any one cell type rather, they are blank cells that can change into different cell types depending on the signals they receive in the body.
A team led by Dr Paul Riley at the UCL Institute of Child Health, has discovered that thymosin ?4 can stimulate new blood vessel generation from progenitor cells from the outermost layer of the adult heart. The research was funded by the British Heart Foundation and the Medical Research Council.
Previously it was thought that cells within the adult heart are in a state of permanent rest and that any progenitor cells that can contribute to heart tissue repair travel into the heart from the bone marrow. This research demonstrates that beneficial cells actually reside in the heart itself.
Dr Riley?s team studied mice bred to lack thymosin ?4 in their hearts. They found that the hearts of these mice did not develop normally, the heart muscle showed early signs of tissue loss and blood vessel development was poor.
Closer examination revealed that without thymosin ?4, the progenitor cells failed to move deeper into the heart and change into the cells needed to build healthy blood vessels and sustain muscle tissue.
??To investigate whether thymosin ?4 could have a therapeutic effect on damaged adult hearts my research team took cells from the outermost layer of adult mouse hearts and grew them in the lab. We found that, when treated with thymosin ?4, these adult cells have as much potential as embryonic cells to create healthy heart tissue. This suggests that thymosin ?4 could have a therapeutic use,?? explained Dr Riley.
Current treatments for a damaged heart are limited by the ability of the adult tissue to respond. By using thymosin ?4 to guide progenitor cells from the outer layer of the heart, to form new blood vessels and nourish tissue, it could be possible to better repair damaged adult hearts.
Dr Riley concluded:
??Our research has shown that blood vessel regeneration is still possible in the adult heart. In the future if we can figure out how to direct the progenitor cells using thymosin ?4, there could be potential for therapy based on the patients? own heart cells. This approach would bypass the risk of immune system rejection, a major problem with the use of stem cell transplants from another source. And, it has the added benefit that the cells are already located in the right place – within the heart itself. All these cells need is the appropriate instructions to guide them towards new blood vessel formation that will help in the repair of muscle damage following a heart attack.??
Professor Jeremy Pearson, Associate Medical Director at the British Heart Foundation, said:
?These results are important and exciting. By identifying for the first time a molecule that can cause cells in the adult heart to form new blood vessels, Dr Riley?s group have taken a large step towards practical therapy to encourage damaged hearts to repair themselves, a goal that researchers are urgently aiming for.?
The Chief Executive of the Medical Research Council, Professor Colin Blakemore commented:
??Finding out how this protein helps to heal the heart offers enormous potential in fighting heart disease, which kills more than 105,000 people in the UK every year. This is an excellent example of the way in which first-class research, at the most basic molecular level, can produce opportunities for translation into innovative new treatments that should help patients and improve their lives.?