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Am J Physiol Lung Cell Mol Physiol 277: L1172-L1178, 1999;
1040-0605/99 $5.00
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Vol. 277, Issue 6, L1172-L1178, December 1999

Hyperoxia inhibits proliferation of Mv1Lu epithelial cells independent of TGF-beta signaling

Raymond C. Rancourt1, Rhonda J. Staversky2, Peter C. Keng3, and Michael A. O'reilly1,2

Departments of 1 Environmental Medicine, 3 Radiation Oncology, and 2 Pediatrics, University of Rochester, Rochester, New York 14642

High concentrations of O2 inhibit epithelial cell proliferation that resumes on recovery in room air. To determine whether growth arrest is mediated by transforming growth factor-beta (TGF-beta ), changes in cell proliferation during exposure to hyperoxia were assessed in the mink lung epithelial cell line Mv1Lu and the clonal variant R1B, which is deficient for the type I TGF-beta receptor. Mv1Lu cells treated with TGF-beta accumulated in the G1 phase of the cell cycle as determined by propidium iodide staining, whereas proliferation of R1B cells was unaffected by TGF-beta . In contrast, hyperoxia inhibited proliferation of both cell lines within 24 h of exposure through an accumulation in the S phase. Mv1Lu cells treated with TGF-beta and exposed to hyperoxia accumulated in the G1 phase, suggesting that TGF-beta can inhibit the S phase accumulation observed with hyperoxia alone. Cyclin A was detected in cultures exposed to room air or growth arrested by hyperoxia while decreasing in cells growth arrested in the G1 phase by TGF-beta . Finally, hyperoxia failed to activate a TGF-beta -dependent transcriptional reporter in both Mv1Lu and R1B cells. These findings reveal that simple growth arrest by hyperoxia involves a defect in S phase progression that is independent of TGF-beta signaling.

proliferation; transforming growth factor-beta


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