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Am J Physiol Lung Cell Mol Physiol 276: L1010-L1017, 1999;
1040-0605/99 $5.00
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Vol. 276, Issue 6, L1010-L1017, June 1999

Mechanisms regulating cAMP-mediated growth of bovine neonatal pulmonary artery smooth muscle cells

Alexandra Guldemeester1, Kurt R. Stenmark2, George H. Brough3, and Troy Stevens3

2 Cardiovascular Pulmonary Research Laboratory and Developmental Biology Laboratories, University of Colorado Health Sciences Center, Denver, Colorado 80262; 1 Department of Pediatric Surgery, Sophia Children's Hospital, 3015 GJ Rotterdam, The Netherlands; and 3 Department of Pharmacology, University of South Alabama College of Medicine, Mobile, Alabama 36688

Neonatal pulmonary artery smooth muscle cells (PASMCs) exhibit enhanced growth capacity and increased growth responses to mitogenic stimuli compared with adult PASMCs. Because intracellular signals mediating enhanced growth responses in neonatal PASMCs are incompletely understood, we questioned whether 1) Gq agonists increase cAMP content and 2) increased cAMP is proproliferative. Endothelin-1 and angiotensin II increased both cAMP content and proliferation in neonatal but not in adult PASMCs. Inhibition of protein kinase C and protein kinase A activity nearly eliminated the endothelin-1- and angiotensin II-induced growth of neonatal PASMCs. Moreover, cAMP increased proliferation in neonatal but not in adult cells. Protein kinase C-stimulated adenylyl cyclase was expressed in both cell types, suggesting that insensitivity to stimulation of cAMP in adult cells was not due to decreased enzyme expression. Our data collectively indicate that protein kinase C stimulation of cAMP is a critical signal mediating proliferation of neonatal PASMCs that is absent in adult PASMCs and therefore may contribute to the unique proproliferative phenotype of these neonatal cells.

adenosine 3',5'-cyclic monophosphate; lung; development; endothelin-1; angiotensin II; signal transduction


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