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Published ahead of print on March 5, 2003, doi:10.1164/rccm.200207-662OC
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American Journal of Respiratory and Critical Care Medicine Vol 167. pp. 1554-1561, (2003)
© 2003 American Thoracic Society

Original Article

Fibroblast Growth Factor Receptor-1 and Neonatal Compensatory Lung Growth after Exposure to 95% Oxygen

Robert P. Jankov, Xiaoping Luo, Ann Campbell, Rosetta Belcastro, Judy Cabacungan, Leslie Johnstone, Helena Frndova, Stephen J. Lye and A. Keith Tanswell

Canadian Institutes of Health Research (CIHR) Group in Lung Development, Lung Biology Programme, Hospital for Sick Children Research Institute; CIHR Group in Developmental and Fetal Health, Samuel Lunenfeld Research Institute, Mt. Sinai Hospital; and Departments of Obstetrics and Gynaecology, Paediatrics, and Physiology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada; and Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China

Correspondence and requests for reprints should be addressed to Dr. A. Keith Tanswell, Division of Neonatology, The Hospital for Sick Children, 555 University Avenue, Toronto, ON, M5G 1X8 Canada. E-mail: keith.tanswell{at}sickkids.ca

Neonatal rats exposed to 95% oxygen (O2) for 7 days from birth had inhibited lung growth, DNA synthesis, and secondary septation. These parameters were rapidly restored by a period of recovery in air. Northern and Western blot analysis and immunohistochemistry were used to screen for the fibroblast growth factor receptor-1 (FGF-R1) and its high affinity ligand, basic fibroblast growth factor (bFGF), which could have a role in this recovery process. Expression of bFGF in the lung was significantly reduced at the end of the 7-day exposure to 95% O2 and was increased after 3 days of recovery in air. Expression of FGF-R1 was not affected by exposure to 95% O2 or recovery in air. We hypothesized that the increase in bFGF after removal from 95% O2, acting through the FGF-R1, would be critical for compensatory growth. Intraperitoneal injection of soluble truncated FGF-R1 at the onset of the recovery phase arrested compensatory lung DNA synthesis and secondary septation seen in control animals after 3 days of recovery, confirming a role for FGF-R1 in this model of compensatory neonatal lung growth.

Key Words: pulmonary oxygen toxicity • bronchopulmonary dysplasia • reactive oxygen species • soluble receptors




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