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Am J Physiol Lung Cell Mol Physiol 282: L1198-L1208, 2002. First published January 4, 2002; doi:10.1152/ajplung.00139.2001
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Vol. 282, Issue 6, L1198-L1208, June 2002

Parathyroid hormone-related protein response to hyperoxic lung injury

Randolph H. Hastings1,2, Rita M. Ryan3, Carl T. D'Angio4, Bruce A. Holm3, Alka Patel3, Rick Quintana1, Elana Biederman1, Douglas W. Burton1,2, and Leonard J. Deftos1,2

1 Research, Anesthesiology, and Medicine Services, Veterans Affairs San Diego Healthcare System, San Diego 92161; 2 Departments of Anesthesiology and Medicine, University of California San Diego, La Jolla, California 92093; 3 Department of Pediatrics (Neonatology), State University of New York at Buffalo, Buffalo 14214; and 4 Department of Pediatrics (Neonatology), Strong Children's Research Center, University of Rochester, Rochester, New York 14642

Parathyroid hormone-related protein (PTHrP) is a growth inhibitor for alveolar type II cells. Type II cell proliferation after lung injury from 85% oxygen is regulated, in part, by a fall in lung PTHrP. In this study, we investigated lung PTHrP after injury induced by >95% oxygen in rats and rabbits. In adult rats, lung PTHrP rose 10-fold over controls to 6,356 ± 710 pg/ml (mean ± SE) at 48 h of hyperoxia. Levels fell to 299 ± 78 pg/ml, and staining for PTHrP mRNA was greatly reduced at 60 h (P < 0.05), the point of most severe injury and greatest pneumocyte proliferation. In adult rabbits, lung PTHrP peaked at 3,289 ± 230 pg/ml after 64 h of hyperoxia with 24 h of normoxic recovery and then dropped to 1,629 ± 153 pg/ml at 48 h of recovery (P < 0.05). Type II cell proliferation peaked shortly after the fall in PTHrP. In newborn rabbits, lavage PTHrP increased by 50% during the first 8 days of hyperoxia, whereas type II cell growth decreased. PTHrP declined at the LD50, concurrent with increased type II cell division. In summary, lung PTHrP initially rises after injury with >95% hyperoxia and then falls near the peak of injury. Changes in PTHrP are temporally related to type II cell proliferation and may regulate repair of lung injury.

adult respiratory distress syndrome; calcitropic hormones; growth factor; receptor; type II pneumocyte


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