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Am J Physiol Lung Cell Mol Physiol (June 28, 2002). doi:10.1152/ajplung.00050.2002
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Articles in PresS, published online ahead of print June 27, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00050.2002
Submitted on February 5, 2002
Accepted on June 15, 2002

Increased epithelial cell proliferation in very premature baboons with chronic lung disease

William M. Maniscalco1*, Richard H. Watkins1, Michael A O'Reilly1, and Colleen P. Shea1

1 Department of Pediatrics, University of Rochester School of Medicine, Rochester, NY, USA

* To whom correspondence should be addressed. E-mail: william_maniscalco{at}urmc.rochester.edu.

Coordinated proliferation of lung cells is required for normal lung growth and differentiation. Chronic lung injury of premature infants may disrupt normal patterns of cell proliferation. To examine patterns of cell proliferation in injured developing lung, we investigated premature baboons delivered at 125 days gestation (~67% of term) and treated with oxygen and ventilation for up to 21 days (PRN group). Each treatment group contained 3-4 animals. During normal in utero lung development, the proportion of proliferating lung cells declined, as measured by the S-phase marker Ki67. In the PRN group, the proportion of proliferating lung cells was 2.5-8.5 fold greater than in gestational controls. By 14 days treatment, the proportion of cells that expressed proSP-B was ~2.5 fold greater than in gestational controls. In the PRN group, 41% of proliferating cells expressed proSP-B, compared to 5.8% in gestational controls. By 21 days treatment, proliferation of proSP-B expressing epithelial cells declined substantially, but the proportion of proliferating non-proSP-B expressing cells increased 7 fold. These data show that the development of CLD is associated with major alterations in normal patterns of lung cell proliferation.




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