Stem Cells and Myocardial Regeneration: Cooperation Wins over Competition
Antagonism between stem cells is not new. Competitive mechanisms are known to be critical for the modulation of organ homeostasis and regeneration. Competitive interaction within the niches results in survival of the fittest stem cells and death of the more vulnerable cells. An upregulation of c-myc transforms cells into "supercompetitors" capable of clonal expansion. The cluster of supercompetitors influences the behavior of the weakest surrounding cells, which are at a growth disadvantage.1 The presence of supercompetitors within niches regulates niche function, and the absence of supercompetitors may alter the preservation of stem cell self-renewal, leading to the generation of old dysfunctional niches.2 However, supercompetitor stem cells may fail to trigger apoptosis in the neighboring aging cells, promoting uncontrolled growth arrest and cellular senescence. This process may become excessive, favoring the formation of crowded niches where old stem cells predominate, opposing the activation of young functionally-competent stem cells. Thus, cooperative cell-to-cell communication may regulate more effectively the fate of stem cells within the niches, since the supporting cells transmit growth signals to stem cells according to the need of the organ and organism.
- Received November 25, 2012.
- Accepted November 27, 2012.
- Copyright © 2012, American Heart Association, Inc. All rights reserved. Unauthorized use prohibited