Published online Feb 21, 2015. doi: 10.3748/wjg.v21.i7.2005
Peer-review started: October 3, 2014
First decision: October 29, 2014
Revised: November 4, 2014
Accepted: January 8, 2015
Article in press: January 8, 2015
Published online: February 21, 2015
Processing time: 133 Days and 0.3 Hours
Epithelial layer of the intestine relies upon stem cells for maintaining homeostasis and regeneration. Two types of stem cells are currently defined in intestinal crypts: the cycling crypt base columnar cells and quiescent cells. Though several candidate markers and regulators of rapidly cycling and quiescent stem cells have been identified so far, the exact nature of quiescent cells is still questionable since investigations mainly focused on candidate markers rather than the label-retaining population itself. Recent results, however, have strengthened the argument for functional plasticity. Using a lineage tracing strategy label-retaining cells (LRCs) of the intestinal epithelium were marked, then followed by a pulse-chase analysis it was found that during homeostasis, LRCs were Lgr5-positive and were destined to become Paneth and neuroendocrine cells. Nevertheless, it was demonstrated that LRCs are capable of clonogenic growth by recall to the self-renewing pool of stem cells in case of epithelial injury. These new findings highlight on the hierarchical and spatial organization of intestinal epithelial homeostasis and the important plasticity of progenitors during tissue regeneration, moreover, provide a motivation for studying their role in disorders like colorectal cancer.
Core tip: The cellular plasticity and lineage reversibility of the epithelial layer may represent adaptive mechanisms for the self-preservation of the epithelial layer after injuries. Recent results revealed that a portion of Lgr5-expressing intestinal cells cycles less frequently, and upon physiological circumstances does not contribute to intestinal homeostasis, however, they reacquire stem cell function and can be recruited to serve as a functional clonogenic stem population after injury.