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1 Lovelace Respiratory Research Institute, Albuquerque, NM, USA
2 The Dow Chemical Company, Midland, MI, USA
3 Department of Pathology and Diagnostic Investigation, Michigan State University, East Lansing, MI, USA
* To whom correspondence should be addressed. E-mail: ytesfaig{at}lrri.org.
Exposures of pulmonary airways to environmental toxins and allergens may cause proliferation of airway epithelial cells, and mucous cell metaplasia (MCM); however, it is unclear to what extent proliferating cells differentiate into mucus-storing cells and contribute to MCM. Our previous studies have demonstrated that Bcl-2, an inhibitor of apoptosis with cell cycle regulatory functions, is expressed in metaplastic mucous cells. The purpose of the present study was to investigate the number of metaplastic mucous cells that are derived from proliferating epithelial cells and whether Bcl-2 has a role in cell cycle entry in these cells. Rats were intratracheally instilled with 100 µg lipopolysaccharide from Pseudomonas aeruginosa in 500 µl saline and proliferating airway cells were labeled with bromodeoxyurindine by implanting a subcutaneous osmotic pump 24 h prior to instillation. The volume of stored mucosubstance and the number of mucous cells were increased 10- and 3-fold, respectively, from 24 to 48 h post instillation. The number of total epithelial cells per mm basal lamina increased and the number of serous cells per mm basal lamina decreased during this time. Approximately 50% of AB/PAS-stained mucous cells were labeled with BrdU at 48 h post-instillation, suggesting that half of the secretory cells were derived from proliferating cells. Furthermore, 50% of the Bcl-2-positive mucous cells were BrdU-negative and therefore derived from nonproliferating, pre-existing cells. Our findings demonstrate that pre-existing and proliferating cells differentiate into mucous cells and compose the LPS-induced metaplasia and that Bcl-2 does not have cell cycle regulatory function in these cells.
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