Histamine activates phospholipase C in human airway epithelial cells via a phorbol ester-sensitive pathway

Am J Physiol. 1996 Oct;271(4 Pt 1):L665-71. doi: 10.1152/ajplung.1996.271.4.L665.

Abstract

In human airway epithelial cell lines 9HTEo- and CFNPE9o, histamine causes a transient elevation of intracellular free calcium concentration ([Ca2+]i) detected by fura 2 fluorescence, which is due to both release from intracellular stores and extracellular Ca2+ entry. The effect of histamine is abolished by the Ca(2+)-ATPase inhibitor thapsigargin. Histamine also stimulates inositol phosphate accumulation. Changes in [Ca2+]i and inositol phosphate production exhibit a similar dose-response relationship for histamine (maximal effect at 10(-4) M), with both phenomena being blocked by the H1 antagonist mepyramine and being insensitive to pertussis toxin treatment. The effects of histamine on phosphoinositide metabolism and [Ca2+]i are abolished by a short-term preincubation with phorbol ester, and this effect is reversed by staurosporine and calphostin C, suggesting a feedback regulation by protein kinase C. The results indicate that human airway epithelial cells contain H1 receptors coupled to phospholipase C through a pertussis toxin-insensitive G protein.

Publication types

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

MeSH terms

  • Calcium / physiology
  • Calcium-Transporting ATPases / antagonists & inhibitors
  • Cell Line
  • Cimetidine / pharmacology
  • Cystic Fibrosis
  • Enzyme Activation / drug effects
  • Enzyme Inhibitors / pharmacology
  • Epithelium / enzymology
  • GTP-Binding Proteins / physiology
  • Histamine / pharmacology*
  • Histamine H1 Antagonists / pharmacology
  • Histamine H2 Antagonists / pharmacology
  • Humans
  • Inositol Phosphates / metabolism
  • Pertussis Toxin
  • Protein Kinase C / physiology
  • Pyrilamine / pharmacology
  • Receptors, Histamine H1 / physiology*
  • Signal Transduction / drug effects
  • Thapsigargin / pharmacology
  • Trachea / cytology
  • Trachea / enzymology*
  • Type C Phospholipases / metabolism*
  • Virulence Factors, Bordetella / pharmacology

Substances

  • Enzyme Inhibitors
  • Histamine H1 Antagonists
  • Histamine H2 Antagonists
  • Inositol Phosphates
  • Receptors, Histamine H1
  • Virulence Factors, Bordetella
  • Thapsigargin
  • Cimetidine
  • Histamine
  • Pertussis Toxin
  • Protein Kinase C
  • Type C Phospholipases
  • GTP-Binding Proteins
  • Calcium-Transporting ATPases
  • Pyrilamine
  • Calcium