Activation of protein kinase A accelerates bovine bronchial epithelial cell migration

John R. Spurzem, Jitendrakumar Gupta, Thomas Veys, Kristen R. Kneifl, Stephen I. Rennard, Todd A. Wyatt

Research output: Contribution to journalArticlepeer-review

43 Scopus citations


Bronchial epithelial cell migration is required for the repair of damaged airway epithelium. We hypothesized that bronchial epithelial cell migration during wound repair is influenced by cAMP and the activity of its cyclic nucleotide-dependent protein kinase, protein kinase A (PKA). We found that, when confluent monolayers of bronchial epithelial cells are wounded, an increase in PKA activity occurs. Augmentation of PKA activity with a cell-permeable analog of cAMP, dibutyryl adenosine 3′,5′-cyclic monophosphate, isoproterenol, or a phosphodiesterase inhibitor accelerated migration of normal bronchial epithelial cells in in vitro wound closure assays and Boyden chamber migration assays. A role for PKA activity was also confirmed with a PKA inhibitor, KT-5720, which reduced stimulated migration. Augmentation of PKA activity reduced the levels of active Rho and the formation of focal adhesions. These studies suggest that PKA activation modulates Rho activity, migration mechanisms, and thus bronchial epithelial repair mechanisms.

Original languageEnglish (US)
Pages (from-to)L1108-L1116
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number5 26-5
StatePublished - 2002


  • Bronchi
  • CAMP
  • Cell movement
  • Epithelial cells

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


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