Jiang T, Sweeney G, Rudolf M T, Klip A, Traynor-Kaplan A, Tsien R Y
Department of Pharmacology and Howard Hughes Medical Institute, University of California San Diego, La Jolla, California 92093-0647, USA.
J Biol Chem. 1998 May 1;273(18):11017-24. doi: 10.1074/jbc.273.18.11017.
Phosphoinositide 3-OH kinases and their products, D-3 phosphorylated phosphoinositides, are increasingly recognized as crucial elements in many signaling cascades. A reliable means to introduce these lipids into intact cells would be of great value for showing the physiological roles of this pathway and for testing the specificity of pharmacological inhibitors of the kinases. We have stereospecifically synthesized di-C8-PIP3/AM and di-C12-PIP3/AM, the heptakis(acetoxymethyl) esters of dioctanoyl- and dilauroylphosphatidylinositol 3,4,5-trisphosphate, in 14 steps from myo-inositol. The ability of these uncharged lipophilic derivatives to deliver phosphatidylinositol 3,4,5-trisphosphate across cell membranes was demonstrated on 3T3-L1 adipocytes and T84 colon carcinoma monolayers. Insulin stimulation of hexose uptake into adipocytes was inhibited by the kinase inhibitor wortmannin and was largely restored by di-C8-PIP3/AM, which had no effect in the absence of insulin. Thus phosphatidylinositol 3,4,5-trisphosphate or a metabolite was necessary but not sufficient for stimulation of hexose transport. In T84 epithelial monolayers, di-C12-PIP3/AM mimicked epidermal growth factor in inhibiting chloride secretion and potassium efflux, suggesting that phosphatidylinositol 3,4, 5-trisphosphate was sufficient to modulate these fluxes and mediate epidermal growth factor's action.
磷酸肌醇3 - 羟基激酶及其产物,即D - 3磷酸化的磷酸肌醇,在许多信号级联反应中越来越被视为关键成分。将这些脂质导入完整细胞的可靠方法,对于阐明该信号通路的生理作用以及测试激酶的药理学抑制剂的特异性具有重要价值。我们从肌醇出发,经过14步立体定向合成了二辛酰基 - 和二月桂酰基磷脂酰肌醇3,4,5 - 三磷酸的七(乙酰氧基甲基)酯,即二 - C8 - PIP3/AM和二 - C12 - PIP3/AM。在3T3 - L1脂肪细胞和T84结肠癌细胞单层上,证明了这些不带电荷的亲脂性衍生物能够跨细胞膜传递磷脂酰肌醇3,4,5 - 三磷酸。激酶抑制剂渥曼青霉素抑制了胰岛素刺激脂肪细胞摄取己糖的过程,而二 - C8 - PIP3/AM在很大程度上恢复了该过程,在无胰岛素的情况下二 - C8 - PIP3/AM没有作用。因此,磷脂酰肌醇3,4,5 - 三磷酸或其代谢产物对于刺激己糖转运是必要的,但并不充分。在T84上皮细胞单层中,二 - C12 - PIP3/AM在抑制氯化物分泌和钾外流方面模拟了表皮生长因子,这表明磷脂酰肌醇3,4,5 - 三磷酸足以调节这些离子通量并介导表皮生长因子的作用。