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Articles in PresS, published online ahead of print July 12, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00053.2002
Submitted on February 6, 2002
Accepted on June 27, 2002
1 Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA
2 Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX, USA
3 Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA; Medical Service, Department of Veteran Affairs Medical Center, Dallas, TX, USA
4 Department of Cardiovascular & Thoracic Surgery, University of Texas Southwestern Medical Center, Dallas, TX, USA
* To whom correspondence should be addressed. E-mail: Connie.Hsia{at}UTSouthwestern.edu.
We examined whether lung growth after pneumonectomy (PNX) invokes normal signaling pathways of postnatal development. We qualitatively and quantitatively assessed the immunoexpression of epidermal growth factor (EGF), its receptor (EGFR), surfactant proteins (SP-A, SP-D, pro SP-B and pro SP-C) and proliferating cell nuclear antigen (PCNA) in immature and mature dog lung. We also assayed these proteins in lungs of immature dogs 3 weeks or 10 months after undergoing right PNX compared to simultaneous matched sham controls. During maturation, alveolar cell proliferation is regionally regulated in parallel with EGF and EGFR levels, and inversely correlated with SP-A and pro SP-C levels. In contrast, post-PNX lung growth is not associated with EGF or EGFR upregulation, but with markedly increased SP-A level and moderately increased SP-D level; pro SP-B and pro SP-C levels did not change. We conclude that a) signaling of EGF axis and differential regulation of surfactant proteins persist during postnatal lung development, b) post-PNX lung growth is not a simple recapitulation of maturational responses, and c) SP-A and SP-D may modulate post-PNX lung growth.
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