Carpentier J L, Sawano F, Geiger D, Gorden P, Perrelet A, Orci L
Institute of Histology and Embryology, University of Geneva Medical Center, Switzerland.
J Cell Physiol. 1989 Mar;138(3):519-26. doi: 10.1002/jcp.1041380311.
Intracellular potassium depletion inhibits receptor-mediated endocytotic processes occurring through clathrin-coated pits. Besides the clathrin-coated pit route, flask-shaped invaginations that do not bear a typical clathrin coat have been recently implicated in receptor-mediated endocytosis of cholera toxin. These invaginations are called "non-coated" to distinguish them from the typical clathrin-coated pits. In the present study, we have investigated whether "non-coated" invaginations are sensitive, as are clathrin-coated pits, to potassium depletion and whether hypertonic medium, which inhibits receptor-mediated endocytosis, also affects "non-coated" invaginations. We found that 1) both potassium depletion and hypertonic medium reduce "non-coated" invaginations on the cell surface; 2) similar to potassium depletion, hypertonic medium markedly decreases the number of clathrin-coated pits; 3) these changes are accompanied by an inhibition of the internalization (measured morphologically) of cholera toxin-gold through "non-coated" invaginations, as well as of alpha 2-macroglobulin-gold taken up by clathrin-coated pits; and 4) in addition, both the hypertonic medium and potassium depletion inhibit the uptake of horseradish peroxidase, a marker of fluid-phase endocytosis.
细胞内钾离子耗竭会抑制通过网格蛋白包被小窝发生的受体介导的内吞过程。除了网格蛋白包被小窝途径外，最近发现没有典型网格蛋白包被的烧瓶状内陷与霍乱毒素的受体介导内吞作用有关。这些内陷被称为“无包被”，以区别于典型的网格蛋白包被小窝。在本研究中，我们调查了“无包被”内陷是否像网格蛋白包被小窝一样对钾离子耗竭敏感，以及抑制受体介导内吞作用的高渗介质是否也会影响“无包被”内陷。我们发现：1）钾离子耗竭和高渗介质都会减少细胞表面的“无包被”内陷；2）与钾离子耗竭类似，高渗介质会显著减少网格蛋白包被小窝的数量；3）这些变化伴随着通过“无包被”内陷对霍乱毒素-金的内化（通过形态学测量）以及通过网格蛋白包被小窝摄取的α2-巨球蛋白-金的抑制；4）此外，高渗介质和钾离子耗竭都会抑制辣根过氧化物酶的摄取，辣根过氧化物酶是液相内吞作用的标志物。
