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Epithelial Progenitor Cells of the Embryonic Lung and the Role of MicroRNAs in Their Proliferation

¹ Department of Cell Biology, Duke University Medical Center, Durham, North Carolina

Correspondence and requests for reprints should be addressed to Brigid Hogan, Ph.D., Department of Cell Biology, Box 3709, Duke University Medical Center, Durham, NC 27710. E-mail: b.hogan{at}cellbio.duke.edu

ABSTRACT

The entire epithelium of the lung is generated from a small pool of undifferentiated progenitor cells. At least during the early stages of development these reside in the distal tips of the embryonic lung. They respond to multiple signals from the surrounding mesenchyme and play a critical role as morphogenetic organizing centers. In addition, they proliferate rapidly and give rise to daughter cells that differentiate into all the specialized epithelial cells types of the newborn lung. Despite the importance of the progenitor cells, we still know relatively little about the mechanisms controlling their proliferation, morphogenesis, and developmental fate. Here, we discuss new data on the potential role of microRNAs in co-coordinately regulating multiple signaling pathways in embryonic progenitor cells. In particular, our recent transgenic experiments suggest that microRNAs encoded by the miR-17-92 cluster positively promote proliferation of epithelial progenitor cells and inhibit their differentiation. We speculate on how this information might be exploited therapeutically in the long term.

Key Words: miR-17-92 • transgenic mouse • Sox9 • NMyc • cancer

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