Kurilova L S, Krutetskaia Z I, Lebedev O E
Tsitologiia. 2007;49(10):858-64.
Using Fura-2AM microfluorimetry the role of phosphatidylinositol kinases in the regulation of Ca2+ signals induced by purinergic agonist ATP and endoplasmic Ca2(+)-ATPase inhibitor thapsigargin in rat peritoneal macrophages was investigated. It was shown that two structurally distinct phosphatidylinositol 3- and phosphatidylinositol-4-kinases inhibitors wortmannin and LY294002 showed a dose- dependent effect on store-dependent Ca2(+)-entry, induced by thapsigargin or ATP. The data suggest that phosphatidylinositol 3- and phosphatidylinositol-4-kinases play an important role in the activation of store-dependent Ca2(+)-entry in macrophages and that their effect might be mediated by their influence on actin cytoskeleton. The results are compatible with the "secretion-like coupling model" for store-dependent Ca2(+)-entry in macrophages based on a reversible trafficking and coupling of the Ca2+ store with the plasma membrane which suggests the involvement of microfilaments and phosphatidylinositol kinases.
运用Fura-2AM显微荧光测定法，研究了磷脂酰肌醇激酶在嘌呤能激动剂ATP和内质网Ca2 + -ATP酶抑制剂毒胡萝卜素诱导的大鼠腹膜巨噬细胞Ca2 +信号调节中的作用。结果表明，两种结构不同的磷脂酰肌醇3激酶和磷脂酰肌醇4激酶抑制剂渥曼青霉素和LY294002对毒胡萝卜素或ATP诱导的储存依赖性Ca2 +内流呈现剂量依赖性效应。数据表明，磷脂酰肌醇3激酶和磷脂酰肌醇4激酶在巨噬细胞储存依赖性Ca2 +内流的激活中起重要作用，其作用可能是通过对肌动蛋白细胞骨架的影响来介导的。这些结果与基于Ca2 +储存与质膜的可逆运输和偶联的巨噬细胞储存依赖性Ca2 +内流的“分泌样偶联模型”相符，这表明微丝和磷脂酰肌醇激酶参与其中。
