Zen K, Biwersi J, Periasamy N, Verkman A S
Department of Medicine, University of California, San Francisco.
J Cell Biol. 1992 Oct;119(1):99-110. doi: 10.1083/jcb.119.1.99.
Acidification of the endosomal pathway is important for ligand and receptor sorting, toxin activation, and protein degradation by lysosomal acid hydrolases. Fluorescent probes and imaging methods were developed to measure pH to better than 0.2 U accuracy in individual endocytic vesicles in Swiss 3T3 fibroblasts. Endosomes were pulse labeled with transferrin (Tf), alpha 2-macroglobulin (alpha 2M), or dextran, each conjugated with tetramethylrhodamine and carboxyfluorescein (for pH 5-8) or dichlorocarboxyfluorescein (for pH 4-6); pH in individual labeled vesicles was measured by ratio imaging using a cooled CCD camera and novel image analysis software. Tf-labeled endosomes acidified to pH 6.2 +/- 0.1 with a t1/2 of 4 min at 37 degrees C, and remained small and near the cell periphery. Dextran- and alpha 2M-labeled endosomes acidified to pH 4.7 +/- 0.2, becoming larger and moving toward the nucleus over 30 min; approximately 15% of alpha 2M-labeled endosomes were strongly acidic (pH less than 5.5) at only 1 min after labeling. Replacement of external Cl by NO3 or isethionate strongly and reversibly inhibited acidification. Addition of ouabain (1 mM) at the time of labeling strongly enhanced acidification in the first 5 min; Tf-labeled endosomes acidified to pH 5.3 without a change in morphology. Activation of phospholipase C by vasopressin (50 nM) enhanced acidification of early endosomes; activation of protein kinase C by PMA (100 nM) enhanced acidification strongly, whereas elevation of intracellular Ca by A23187 (1 microM) had no effect on acidification. Activation of protein kinase A by CPT-cAMP (0.5 mM) or forskolin (50 microM) inhibited acidification. Lysosomal pH was not affected by ouabain or the protein kinase activators. These results establish a methodology for quantitative measurement of pH in individual endocytic vesicles, and demonstrate that acidification of endosomes labeled with Tf and alpha 2M (receptor-mediated endocytosis) and dextran (fluid-phase endocytosis) is sensitive to intracellular anion composition, Na/K pump inhibition, and multiple intracellular second messengers.
内体途径的酸化对于配体和受体分选、毒素激活以及溶酶体酸性水解酶介导的蛋白质降解至关重要。已开发出荧光探针和成像方法来测量pH值,在瑞士3T3成纤维细胞的单个内吞小泡中测量精度优于0.2 U。用转铁蛋白(Tf)、α2巨球蛋白(α2M)或葡聚糖对内体进行脉冲标记,每种都与四甲基罗丹明和羧基荧光素(用于pH 5 - 8)或二氯羧基荧光素(用于pH 4 - 6)偶联;使用冷却的电荷耦合器件(CCD)相机和新型图像分析软件通过比率成像测量单个标记小泡中的pH值。在37℃下,Tf标记的内体酸化至pH 6.2±0.1,t1/2为4分钟,并保持较小且靠近细胞周边。葡聚糖和α2M标记的内体酸化至pH 4.7±0.2,在30分钟内变得更大并向细胞核移动;在标记后仅1分钟,约15%的α2M标记的内体呈强酸性(pH小于5.5)。用硝酸根或羟乙基磺酸根替代外部氯离子可强烈且可逆地抑制酸化。在标记时添加哇巴因(1 mM)在最初5分钟内强烈增强酸化;Tf标记的内体酸化至pH 5.3,形态无变化。血管加压素(50 nM)激活磷脂酶C增强早期内体的酸化;佛波酯(PMA,100 nM)激活蛋白激酶C强烈增强酸化,而A23187(1 μM)升高细胞内钙离子浓度对酸化无影响。CPT - cAMP(0.5 mM)或福斯可林(50 μM)激活蛋白激酶A抑制酸化。溶酶体pH不受哇巴因或蛋白激酶激活剂的影响。这些结果建立了一种定量测量单个内吞小泡中pH值的方法,并证明用Tf和α2M(受体介导的内吞作用)以及葡聚糖(液相内吞作用)标记 的内体酸化对细胞内阴离子组成、钠钾泵抑制和多种细胞内第二信使敏感。