Adenosine A2B receptor signalling is altered by stimulation of bradykinin or interleukin receptors in astroglioma cells

Neurochem Int. 1994 Jul;25(1):99-102. doi: 10.1016/0197-0186(94)90060-4.

Abstract

The human astroglioma cell D384 possesses adenosine A2B receptors coupled to the formation of cyclic AMP. These cells also possess bradykinin B2 receptors coupled to phospholipase C and consequent increases in intracellular calcium and protein kinase C. Interleukin 1 beta causes an increase in c-fos, AP-1 transcriptional activity and an increased expression of several genes including NGF, but the initial signalling events are unknown. Bradykinin causes a rapid decrease in A2B receptor mediated cAMP formation, via a mechanism that involves calcium, but not cGMP, and appears to depend upon a direct decrease in adenylyl cyclase. Il-1 beta causes a slowly developing (18-24 h) increase in A2B receptor signalling. The results indicate that adenosine effects in glial cells, believed to be important in neuroprotection, are modified in the short and long-term by inflammatory mediators.

MeSH terms

  • Astrocytoma / metabolism*
  • Bradykinin / pharmacology
  • Brain Neoplasms / metabolism*
  • Calcium / metabolism
  • Cyclic AMP / metabolism
  • Humans
  • Inositol 1,4,5-Trisphosphate / metabolism
  • Interleukin-1 / pharmacology
  • Interleukins / pharmacology
  • Proto-Oncogene Proteins c-fos / biosynthesis
  • Receptors, Bradykinin / metabolism*
  • Receptors, Interleukin / metabolism*
  • Receptors, Purinergic P1 / physiology*
  • Signal Transduction / drug effects
  • Signal Transduction / physiology*
  • Tumor Cells, Cultured

Substances

  • Interleukin-1
  • Interleukins
  • Proto-Oncogene Proteins c-fos
  • Receptors, Bradykinin
  • Receptors, Interleukin
  • Receptors, Purinergic P1
  • Inositol 1,4,5-Trisphosphate
  • Cyclic AMP
  • Bradykinin
  • Calcium