Protein Helps Heart Repair Itself

New research has found cells in the outer layer of the heart possess the ability to migrate deeper into the organ to carry out necessary repairs. A protein called thymosin beta 4 controls this migration of progenitor cells. Thymosin beta 4 is already known to help reduce muscle cell loss after a heart attack.

This discovery of cell migration opens up the possibility of developing more effective treatments for heart disease by using the protein. Progenitor cells can convert into different types of adult cells; this makes them similar to stem cells. However there was no known source of these cells in the heart so far and they had to be extracted from the bone marrow to effect repairs.

Published in the journal Nature, this latest research by scientists at University College London (UCL) is the first to discover presence of progenitor cells within the heart tissue itself. The researchers discovered progenitor cells in the outermost layer of the heart can be stimulated under the influence of thymosin ß4 to form new blood vessels.

Mice lacking thymosin ß4 in their hearts were bred for the study. It was found these mice failed to develop normal hearts. Early signs of tissue loss in the heart muscle and poor blood vessel development were also observed. When they examined the mice closely, researchers found the progenitor cells had failed to move deeper into the heart on account of lack of thymosin ß4. This had inhibited growth of cells needed to build healthy blood vessels and sustain muscle tissue.

Researchers then took cells from the outer layer of the hearts of these adult mice and grew them in the lab to check if the protein could help repair damaged adult hearts. Lead researcher Dr. Paul Riley said, “We found that, when treated with thymosin ß4, these adult cells have as much potential as embryonic cells to create healthy heart tissue.” Dr. Riley believes it is possible to find a more effective way to repair damaged heart with the use of thymosin ß4.

“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,” he said.

Commenting further, he said, “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.”

The study was funded by the British Heart Foundation (BHF) and the Medical Research Council (MRC). Professor Jeremy Pearson, BHF Associate Medical Director stated, “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 has taken a large step towards practical therapy to encourage damaged hearts to repair themselves, a goal that researchers are urgently aiming for.”

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