PKA induces Ca2+ release and enhances ciliary beat frequency in a Ca2+-dependent and -independent manner

Alex Braiman, Orna Zagoory, Zvi Priel

Research output: Contribution to journalArticlepeer-review

44 Scopus citations

Abstract

The intent of this work was to evaluate the role of cAMP in regulation of ciliary activity in frog mucociliary epithelium and to examine the possibility of cross talk between the cAMP- and Ca2+dependent pathways in that regulation. Forskolin and dibutyryl cAMP induced strong transient intracellular Ca2+ concentration ([Ca2+](i)) elevation and strong ciliary beat frequency enhancement with prolonged stabilization at an elevated plateau. The response was not affected by reduction of extracellular Ca2+ concentration. The elevation in [Ca2+](i) was canceled by pretreatment with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-AM, thapsigargin, and a phospholipase C inhibitor, U-73122. Under those experimental conditions, forskolin raised the beat frequency to a moderately elevated plateau, whereas the initial strong rise in frequency was completely abolished. All effects were canceled by H-89, a selective protein kinase A (PKA) inhibitor. The results suggest a dual role for PKA in ciliary regulation. PKA releases Ca2+ from intracellular stores, strongly activating ciliary beating, and, concurrently, produces moderate prolonged enhancement of the beat frequency by a Ca2+independent mechanism.

Original languageEnglish
Pages (from-to)C790-C797
JournalAmerican Journal of Physiology - Cell Physiology
Volume275
Issue number3 44-3
DOIs
StatePublished - 1 Jan 1998

Keywords

  • Adenosine 3',5'-cyclic monophosphate
  • Adenylyl cyclase
  • Cilia
  • Intracellular calcium pools
  • Phospholipase C
  • Protein kinase A

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