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1 Department of Pediatrics School of Medicine and Dentistry, The University of Rochester, Rochester, NY, USA
* To whom correspondence should be addressed. E-mail: michael_oreilly{at}urmc.rochester.edu.
Aberrant pulmonary epithelial and mesenchymal cell proliferation occurs when newborns are treated with oxygen and ventilation to mitigate chronic lung disease. Because the cyclin-dependent kinase inhibitor p21 inhibits proliferation of oxygen-exposed cells, its expression was investigated in premature baboons delivered at 125 days (67% of term) and treated with oxygen and ventilation pro re nata (PRN) for 2, 6, 14 and 21 days. Approximately 5% of all cells expressed p21 during normal lung development of which less than 1% of these cells were proSP-B positive epithelial cells. The percentage of cells expressing p21 increased 3-fold in all PRN treated animals, but different cell populations expressed it during disease progression. Between 2 and 6 days of treatment, p21 was detected in 30 to 40% of proSP-B cells. In contrast, only 12% of proSP-B cells expressed p21 by 14 and 21 days of treatment, by which time p21 was also detected in mesenchymal cells. Even though increased epithelial and mesenchymal cell proliferation occurs during disease progression, those cells expressing p21 did not also express the proliferative marker Ki67. Thus, two populations of epithelial and mesenchymal cells can be identified that are either expressing Ki67 and proliferating or expressing p21 and not proliferating. These data suggest that p21 may play a role in disorganized proliferation and alveolar hypoplasia seen in newborn chronic lung disease.
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