Nuclear accumulation of G-actin in isolated rat hepatocytes by adenine nucleotides

Biochem Biophys Res Commun. 1997 Nov 26;240(3):697-700. doi: 10.1006/bbrc.1997.7724.

Abstract

Extracellular ATP induces bleb formation in isolated rat hepatocytes. We examined the effect of extracellular ATP on the actin cytoskeleton of these hepatocytes. Exposure to 100 microM ATP caused pronounced nuclear accumulation of G-actin. ADP, AMP, adenosine, and dibutyryl-cAMP induced the same effect. Adenosine deaminase could inhibit both ATP- and adenosine-induced nuclear accumulation. The P2-receptor agonists, UTP and 2' & 3'-O-(4-benzoylbenzoyl)-adenosine 5'-triphosphate, did not induce this redistribution of G-actin. Phalloidin, which prevents depolymerisation of F-actin filaments to G-actin monomers, inhibited adenosine-induced nuclear accumulation of G-actin. These observations suggest that nuclear accumulation of G-actin is mediated by adenosine receptors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism*
  • Adenine Nucleotides / pharmacology*
  • Adenosine / pharmacology
  • Adenosine Deaminase / metabolism
  • Adenosine Triphosphate / analogs & derivatives
  • Adenosine Triphosphate / pharmacology
  • Animals
  • Cell Nucleus / metabolism*
  • Cells, Cultured
  • Cytoskeleton / metabolism
  • Liver / cytology
  • Liver / drug effects
  • Liver / metabolism*
  • Microscopy, Confocal
  • Phalloidine / pharmacology
  • Purinergic P2 Receptor Agonists
  • Rats
  • Receptors, Purinergic P2 / metabolism
  • Uridine Triphosphate / pharmacology

Substances

  • Actins
  • Adenine Nucleotides
  • Purinergic P2 Receptor Agonists
  • Receptors, Purinergic P2
  • Phalloidine
  • Adenosine Triphosphate
  • Adenosine Deaminase
  • Adenosine
  • Uridine Triphosphate