Cardiac Stem Cell Migration Dependent on p38

Wuhan, China -

Many tissues have tissue resident stem cells. Although not in high numbers, these stem cells have nevertheless been demonstrated to play at least some role in regeneration after injury. Stem cells in tissues can be isolated by their side population characteristics, or by their expression of aldehyde dehydrogenase or by expression of markers such as c-kit or CD133.

One interesting question is how migration of tissue specific stem cells occurs after tissue injury. It is known that various signals such as SDF-1 and VEGF cause mobilization of bone marrow stem cells after heart attacks, but what signals cause mobilization of cardiac tissue stem cells to the area of infarct? This question was addressed in a recent publication (Kuang et al. Stem cell factor/c-kit signaling mediated cardiac stem cell migration via activation of p38 MAPK. Basic Res Cardiol. 2007 Dec 17).

The investigators induced heart attacks in rats by occluding the blood vessels feeding the left myocardium and did time course analysis of cytokines upregulated. It was found that SDF-1 expression peaked on day 5 after the heart attack.

Cardiac stem cells were isolated and migration was assessed towards a gradient of SDF-1. Migration could be blocked by inhibition of p38. It is important to emphasize that p38 blockade actually suppressed responsiveness of the cells to SDF-1. These data suggest that similar signals that induce bone marrow stem cell migration to injured tissue may be involved in the stimulation of migration of tissue resident stem cells to the area of injury.