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

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.