Dr. Li's team used genetically-engineered mice in which bone marrow cells were modified to carry a green fluorescent marker allowing researchers to easily track them. The researchers demonstrated that these bone marrow cells are quickly mobilized to the damaged heart region following a heart attack. Once in the damaged area, the cells produce chemicals that trigger the growth of new blood vessels--an important step in repairing the injured heart.
The research also demonstrated that a specific molecule, called c-kit, which is located on the surface of a subset of bone marrow cells, plays a central role in this mobilization. The molecule c-kit is the 'switch' that needs to be turned on by the 'SOS signals' sent by the damaged heart. By binding to another molecule called the stem cell factor ?much like a lock and key -- the "turned on" c-kit activates the bone marrow cells to migrate to the heart to help stimulate new blood vessel growth.
In the study, mice with defective c-kit bone marrow cells, could not mobilize these cells to race towards the injured site and regenerate the injured heart. Their heart function was dramatically impaired and, 42 days after a heart attack, their hearts dilated to twice the size of the normal mouse heart. However, the heart function of the c-kit defective mice could be restored to normal by restoring the c-kit cells in their bone marrow, confirming the importance of these cells in repairing the heart. This suggests that a similar treatment of an infusion of bone marrow cells after a heart attack may prevent progression of heart failure in patients who survived a heart attack.
The study may explain why some pati