Modulation of calcium signaling by interleukin-13 in human airway smooth muscle: role of CD38/cyclic adenosine diphosphate ribose pathway

Am J Respir Cell Mol Biol. 2004 Jul;31(1):36-42. doi: 10.1165/rcmb.2003-0313OC. Epub 2004 Feb 5.

Abstract

CD38/cyclic adenosine diphosphate ribose (cADPR) signaling plays an important role in the regulation of intracellular calcium responses to agonists in a variety of cells, including airway smooth muscle (ASM) cells. The present study was aimed at determining the effect of interleukin (IL)-13, a cytokine implicated in the pathogenesis of asthma, on CD38/cADPR signaling and to ascertain the contribution of CD38/cADPR signaling to IL-13-induced airway hyperresponsiveness. Human ASM cells maintained in culture were exposed to 50 ng/ml IL-13 for 22 h and levels of CD38 expression and intracellular calcium responses to agonists were measured. Treatment of human ASM cells with IL-13 resulted in increased CD38 expression as determined by real-time polymerase chain reaction, Western blot analysis, and indirect immunofluorescence. Increased CD38 expression was reflected as increased ADP-ribosyl cyclase activity in the ASM cell membranes. The net intracellular calcium responses to bradykinin, thrombin, and histamine were significantly (P < or = 0.05) higher in cells treated with IL-13 compared with controls. Furthermore, 8-bromo-cADPR, a cADPR antagonist, attenuated IL-13-induced augmented intracellular calcium responses to agonists in human ASM cells. These findings indicate that the CD38/cADPR-dependent pathway has a major role in IL-13-induced modulation of calcium signaling in human ASM.

Publication types

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

MeSH terms

  • ADP-ribosyl Cyclase / immunology
  • ADP-ribosyl Cyclase / physiology*
  • ADP-ribosyl Cyclase 1
  • Antigens, CD / immunology
  • Antigens, CD / physiology*
  • Asthma / immunology
  • Asthma / metabolism
  • Asthma / physiopathology
  • Bronchi / immunology
  • Bronchi / metabolism*
  • Bronchi / physiopathology
  • Bronchial Hyperreactivity / immunology
  • Bronchial Hyperreactivity / metabolism
  • Bronchial Hyperreactivity / physiopathology
  • Bronchoconstriction / drug effects
  • Bronchoconstriction / physiology
  • Bronchoconstrictor Agents / pharmacology
  • Calcium / metabolism
  • Calcium Signaling / drug effects
  • Calcium Signaling / immunology*
  • Cell Membrane / drug effects
  • Cell Membrane / immunology
  • Cell Membrane / metabolism
  • Cells, Cultured
  • Cyclic ADP-Ribose / analogs & derivatives
  • Cyclic ADP-Ribose / antagonists & inhibitors
  • Cyclic ADP-Ribose / metabolism
  • Cyclic ADP-Ribose / pharmacology
  • Humans
  • Interleukin-13 / immunology
  • Interleukin-13 / metabolism*
  • Interleukin-13 / pharmacology
  • Intracellular Fluid / drug effects
  • Intracellular Fluid / metabolism
  • Membrane Glycoproteins
  • Muscle, Smooth / immunology
  • Muscle, Smooth / metabolism*
  • Muscle, Smooth / physiopathology
  • Myocytes, Smooth Muscle / drug effects
  • Myocytes, Smooth Muscle / immunology
  • Myocytes, Smooth Muscle / metabolism*
  • Up-Regulation / drug effects
  • Up-Regulation / immunology

Substances

  • Antigens, CD
  • Bronchoconstrictor Agents
  • Interleukin-13
  • Membrane Glycoproteins
  • Cyclic ADP-Ribose
  • ADP-ribosyl Cyclase
  • CD38 protein, human
  • ADP-ribosyl Cyclase 1
  • Calcium