Improving mouse heart function following heart attack
The team, led by Katsuhisa Matsuura and Issei Komuro, found that CPCs not only formed heart muscle cells but also secreted a soluble molecule (sVCAM-1) that induced the migration of endothelial cells (which help form new blood vessels) and CPCs and prevented heart muscle cells dying from oxidative stress. In the mouse model of heart attack, preventing sVCAM-1 from binding to the protein VLA-4 inhibited the formation of new blood vessels and blocked CPC migration and survival, leading to a decreased ability of the transplanted CPC sheets to improve heart function. The authors conclude that these data provide new insight into the mechanisms by which heart stem/progenitor cells improve heart function following heart attack.
TITLE: Transplantation of cardiac progenitor cells ameliorates cardiac dysfunction after myocardial infarction in mice
Source: Journal of Clinical Investigation