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Adult heart cells learn to heal

Adult heart cells learn to heal

15 November 2006

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 ß4, a protein already known for its ability to reduce muscle cell loss after heart attack, can instruct the heart to heal itself.

Fluorescent image of a section through an adult mouse heart, the muscle cells of the heart are shown in blue. The outer layer of progenitor cells and the blood vessels which nourish the muscle tissue are highlighted in red

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 ß4 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 ß4 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 ß4, 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 ß4 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 ß4, these adult cells have as much potential as embryonic cells to create healthy heart tissue. This suggests that thymosin ß4 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 ß4 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 ß4, 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.”
  • Notes to editors
  • 1. Thymosin β4 induces adult epicardial progenitor mobilization and neovascularisztion. Advance online publication in Nature on 15th November 2006
  • 2. The research was funded by the British Heart Foundation and the Medical Research Council.
  • 3. Dr Paul Riley is based in the University College London Institute of Child Health at Great Ormond Street Hospital, London.
  • 4. The British Heart Foundation (BHF) is leading the battle against heart and circulatory disease - the UK’s biggest killer. The Charity is a major funder and authority in cardiovascular research. It plays an important role in funding education, both of the public and of health professionals, and in providing life-saving cardiac equipment and support for rehabilitation and care. For more information visit bhf.org.uk
  • 5. The Medical Research Council (MRC) is funded by the UK tax-payer. It aims to improve human health. The research it supports and the scientists it trains meet the needs of the health services, the pharmaceutical and other health-related industries and universities. The MRC has funded work which has led to some of the most significant discoveries and achievements in medicine in the UK. http://www.mrc.ac.uk
  • 6. The UCL Institute of Child Health is, with Great Ormond Street Hospital, the largest centre for paediatric research and training outside the Americas. Rated 5*A, the highest mark for research quality, it is one of only four clinical research institutes to achieve this.
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