Myocardial infarction leads to loss of tissue and impairment of cardiac per
formance. The remaining myocytes are unable to reconstitute the necrotic ti
ssue, and the post-infarcted heart deteriorates with time(1). Injury to a t
arget organ is sensed by distant stem cells, which migrate to the site of d
amage and undergo alternate stem cell differentiation(2-5); these events pr
omote structural and functional repair(6-8). This high degree of stem cell
plasticity prompted us to test whether dead myocardium could be restored by
transplanting bone marrow cells in infarcted mice. We sorted lineage-negat
ive (Lin(-)) bone marrow cells from transgenic mice expressing enhanced gre
en fluorescent protein(9) by fluorescence-activated cell sorting on the bas
is of c-kit expression(10). Shortly after coronary ligation, Lin(-) c-kit(P
OS) cells were injected in the contracting wall bordering the infarct. Here
we report that newly formed myocardium occupied 68% of the infarcted porti
on of the ventricle 9 days after transplanting the bone marrow cells. The d
eveloping tissue comprised proliferating myocytes and vascular structures.
Our studies indicate that locally delivered bone marrow cells can generate
de novo myocardium, ameliorating the outcome of coronary artery disease.