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The Proceedings of the American Thoracic Society 5:360 (2008)
© 2008 The American Thoracic Society
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Epithelial Progenitor Cells in Lung Development and Repair

Emma L. Rawlins1 and Brigid L. M. Hogan1

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

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

The goal of stem cell–based therapies is to either stimulate endogenous stem cells or to supply exogenous cells to mediate the repair of a damaged tissue. Several putative adult epithelial stem cells have been identified in the mouse model system. However, their capacity to mediate repair, and the mechanisms that control this, remain unclear. Also, the time at which they arise during development, and their relationship to embryonic progenitor cells, are not known.

Id2 (Inhibitor of differentiation 2) is a negative regulator of the bHLH family of transcription factors. During branching morphogenesis of the mouse lung, Id2 is very strongly expressed in the putative multipotent epithelial progenitor cell population in the distal epithelial tips. These cells are thought to give rise to both proximal conducting airway and distal alveolar epithelial cell types. We have targeted the endogenous Id2 locus to replace the coding region with either eGFP or an inducible form of the Cre DNA recombinase (CreER2T). We are using these "knock in" mice to follow the descendents of the Id2-expressing cells during different stages of lung development and in the normal and injured adult lung. Our preliminary results show that the Id2+ epithelial cells in the branching lung are indeed a multipotent progenitor population whose descendents are capable of giving rise to all epithelial lineages. Moreover, we have shown that this Id2+ progenitor cell population is maintained throughout the canalicular stage of lung development. During this later developmental phase, the fate of its daughters becomes restricted to alveolar cell types.

FOOTNOTES

Supported by Parker B. Francis Foundation Fellowship to E.L.R. and NIH grant 080517 to B.L.M.H.

Conflict of Interest Statement: Neither of the authors has a financial relationship with a commercial entity that has an interest in the subject of this manuscript.

(Received in original form August 16, 2007; accepted in final form October 16, 2007)





This Article
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Right arrow Articles by Rawlins, E. L.
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Right arrow Articles by Rawlins, E. L.
Right arrow Articles by Hogan, B. L. M.

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