Heart attacks are a common medical risk, especially as people become older. When a heart attack happens, and the person survives, the cells that make up the heart, cardiomyocytes, are damaged. This occurs due a temporary lack of oxygen. The damaged cells, which act as cardiac muscle cells, weaken the patient.
There are two types of cells within the heart: the cardiomyocytes and the cardiac pacemaker cells. Cardiomyocytes shape the fundamental contractile units of muscle cells. Cardiac pacemaker cells help to control the heart rate.
Due to the damage and associated risks, biomedical scientists have examined whether heart cells can be repaired using stem cells. The theory is that stems cells could possibly be transplanted into the wall of heart muscle, together with native heart muscle cells, with the aim of improving contractile function.
Progress using stem cells has been slow, due to a number of ineffective results. The pairing of the heart cells is structurally strong, but there is a difference with contractile strength, with the cells made from stem-cells being weaker.
In order to assist data review, Harvard University researchers have developed a system to measure the relationship between native heart cardiomyocytes and stem-cell derived cardiomyocytes. The researchers have deployed mouse models to examine the process. This has revealed that the two cell-types (native cardiomyocytes and stem-cell derived cardiomyocytes) combine to create “two-cell microtissue.” The researchers have dubbed this “muscle on-a-chip.”
This has led to the finding that the differences in contractile strength between the two cell-types is due to misdirected transmission of mechanical forces, with forces directed outwards rather than between the coupled cells.
The new knowledge about mechanical coupling of stem cells and native cells provides the basis for improving the use of stem-derived cells with an aim of improving patient outcomes.
The research findings are published in The Journal of Cell Biology. The research paper is titled ‘Coupling primary and stem cell–derived cardiomyocytes in an in vitro model of cardiac cell therapy.’
