Involvement of a signal transduction mechanism in ATP-induced mucin release from cultured airway goblet cells

Am J Respir Cell Mol Biol. 1993 Feb;8(2):121-5. doi: 10.1165/ajrcmb/8.2.121.


Release of mucins from cultured airway surface epithelial cells can be stimulated by extracellular ATP via a P2-purinergic receptor-mediated mechanism (K. C. Kim and B. C. Lee. 1991. Br. J. Pharmacol. 103:1053-1056). In this report, we studied the mechanism by which extracellular ATP induces the mucin release. We found that: (1) ATP increased both mucin release and generation of inositol phosphates in a dose-dependent fashion, and their dose-effect relationships were almost superimposed; (2) the increases in both mucin release and the phosphatidylinositol phosphate (PI) turnover by extracellular ATP were partially, but almost equally, blocked by the pretreatment with pertussis toxin (42% for mucin release and 44% for PI turnover). We conclude that in cultured airway goblet cells extracellular ATP stimulates mucin release by a signal transduction mechanism, which seems to involve coupling of ATP-activated P2 purinoceptors with phospholipase C, at least in part, via pertussis toxin-sensitive GTP-binding proteins. This may be an important finding in understanding the regulation of mucin release by airway goblet cells, since a number of agents present in the airway could influence this signal transduction pathway and subsequently modulate the mucin secretion.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenosine Triphosphate / metabolism*
  • Animals
  • Cells, Cultured
  • Cricetinae
  • Enzyme Activation
  • GTP-Binding Proteins / metabolism
  • Inositol Phosphates / biosynthesis
  • Male
  • Mesocricetus
  • Mucins / metabolism*
  • Receptors, Purinergic / metabolism
  • Signal Transduction*
  • Trachea / cytology
  • Trachea / enzymology
  • Trachea / metabolism*
  • Type C Phospholipases / metabolism


  • Inositol Phosphates
  • Mucins
  • Receptors, Purinergic
  • Adenosine Triphosphate
  • Type C Phospholipases
  • GTP-Binding Proteins