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Heart can carry out its own repairs
Scientists have shown that cells in the heart’s outer layer can migrate deeper into a failing organ to carry out essential repairs.
The migration of progenitor cells is controlled by a protein called thymosin ß4, already known to help reduce muscle cell loss after a heart attack. The discovery opens up the possibility of using the protein to develop more effective treatments for heart disease. The University College London (UCL) study appears in the journal Nature. Progenitor cells are similar to stem cells, in that they have the potential to turn into different types of adult tissue.
However, it had been thought there was no ready source of these cells in the heart, and to carry out repairs they had to be summoned up from the bone marrow. The latest research is the first to show that they actually reside within the heart tissue itself. The UCL team discovered under the influence of thymosin ß4, progenitor cells in the outermost layer of the heart can be stimulated to form new blood vessels.
The researchers bred mice lacking thymosin ß4 in their hearts. They found 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.
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