Modulation of endothelin-induced intracellular Ca2+ mobilization by interleukin-1 beta and lipopolysaccharide in C6 rat glioma cells

Neuropeptides. 1997 Apr;31(2):187-92. doi: 10.1016/s0143-4179(97)90088-3.

Abstract

We have investigated the effects of interleukin (IL)-1 beta and lipopolysaccharide (LPS) on endothelin (ET)-induced intracellular Ca2+ rise in C6 rat glioma cells in order to study the mechanisms of their effects on Ca2+ signaling systems. Pretreatment with IL-1 beta (10(3) U/mL) and LPS (1 microgram/mL) for 24 h significantly inhibited 100 nM ET-1-induced increase in intracellular Ca2+ either in the presence or absence of external Ca2+. Their inhibitory effects were in dosedependent (IL-1 beta; 50-1000 U/mL, LPS; 10-1000 ng/mL) and time-dependent (12-24 h) manners. A tyrosine kinase antagonist genistein (50 microM) but not a protein kinase C inhibitor H7 (30 microM) prevented the inhibition of the ET response by IL-1 beta and LPS. These results suggest that activation of tyrosine kinase may be essential for the inhibition of the ET receptor-mediated Ca2+ signaling systems by IL-1 beta and LPS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / pharmacology
  • Animals
  • Calcium / metabolism*
  • Endothelin-1 / pharmacology*
  • Enzyme Inhibitors / pharmacology
  • Genistein
  • Glioma
  • Interleukin-1 / pharmacology*
  • Isoflavones / pharmacology
  • Kinetics
  • Lipopolysaccharides / pharmacology*
  • Protein-Tyrosine Kinases / antagonists & inhibitors
  • Rats
  • Tumor Cells, Cultured

Substances

  • Endothelin-1
  • Enzyme Inhibitors
  • Interleukin-1
  • Isoflavones
  • Lipopolysaccharides
  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
  • Genistein
  • Protein-Tyrosine Kinases
  • Calcium