Meijerman I, Blom W M, de Bont H J, Mulder G J, Nagelkerke J F
Division of Toxicology, Leiden-Amsterdam Center for Drug Research, Leiden University, The Netherlands.
Biochem Biophys Res Commun. 1997 Nov 26;240(3):697-700. doi: 10.1006/bbrc.1997.7724.
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.
细胞外ATP可诱导离体大鼠肝细胞形成气泡。我们研究了细胞外ATP对这些肝细胞肌动蛋白细胞骨架的影响。暴露于100微摩尔ATP会导致G-肌动蛋白在细胞核中显著积累。ADP、AMP、腺苷和二丁酰环磷腺苷也会产生相同的效果。腺苷脱氨酶可抑制ATP和腺苷诱导的细胞核积累。P2受体激动剂UTP和2',3'-O-(4-苯甲酰苯甲酰基)-腺苷5'-三磷酸不会诱导G-肌动蛋白的这种重新分布。鬼笔环肽可防止F-肌动蛋白丝解聚为G-肌动蛋白单体，它抑制了腺苷诱导的G-肌动蛋白在细胞核中的积累。这些观察结果表明，G-肌动蛋白在细胞核中的积累是由腺苷受体介导的。
