Watanabe S, Phillips M J
Proc Natl Acad Sci U S A. 1984 Oct;81(19):6164-8. doi: 10.1073/pnas.81.19.6164.
Cytoplasmic microinjection of Ca2+ triggers contraction of bile canaliculi in freshly isolated monolayer cultures of rat hepatocytes. Unseparated paired hepatocytes were used to demonstrate this motility-based phenomenon. Only one cell of the pair was injected, but fluorescein spread from the target cell to the opposite cell; also, the contractions were always uniform, equally involving both hepatocytes that form the canaliculus, indicating that communication exists between the cell pairs. Inhibitors of calmodulin and actin filaments, trifluoperazine and cytochalasin B, respectively, inhibited the Ca2+-induced contractions. Hence, the mechanism of contraction has features in common with actin-myosin based cytoplasmic motility behavior found in other non-muscle cells.
向大鼠肝细胞新鲜分离的单层培养物的胆小管中进行细胞质微量注射Ca2+会引发其收缩。未分离的成对肝细胞被用于证明这种基于运动的现象。仅对成对细胞中的一个进行注射,但荧光素会从靶细胞扩散到相对的细胞;此外,收缩总是均匀的,同样涉及形成胆小管的两个肝细胞,这表明细胞对之间存在通讯。钙调蛋白和肌动蛋白丝的抑制剂,即三氟拉嗪和细胞松弛素B,分别抑制了Ca2+诱导的收缩。因此,收缩机制具有与在其他非肌肉细胞中发现的基于肌动蛋白-肌球蛋白的细胞质运动行为相同的特征。