Tulapurkar M E, Schäfer R, Hanck T, Flores R V, Weisman G A, González F A, Reiser G
Institut für Neurobiochemie, Medizinische Fakultät, Otto-von-Guericke-Universität, Leipziger Strasse 44, 39120 Magdeburg, Germany.
Cell Mol Life Sci. 2005 Jun;62(12):1388-99. doi: 10.1007/s00018-005-5052-0.
Extracellular nucleotides exert a large number of physiological effects through activation of P2Y receptors. We expressed rat P2Y2 (rP2Y2) receptor, tagged with green fluorescent protein (GFP) in HEK-293 cells and visualized receptor translocation in live cells by confocal microscopy. Functional receptor expression was confirmed by determining [Ca2+]i responses. Agonist stimulation caused a time-dependent translocation of the receptor from the plasma membrane to the cytoplasm. Rearrangement of the actin cytoskeleton was observed during agonist-mediated rP2Y2-GFP receptor internalization. Colocalization of the internalized receptor with early endosomes, clathrin and lysosomes was detected by confocal microscopy. The inhibition of receptor endocytosis by either high-density medium or chlorpromazine in the presence of UTP indicates that the receptor was internalized by the clathrin-mediated pathway. The caveolin-mediated pathway was not involved. Targeting of the receptor from endosomes to lysosomes seems to involve the proteasome pathway, because proteasomal inhibition increased receptor recycling back to the plasma membrane.
细胞外核苷酸通过激活P2Y受体发挥大量生理效应。我们在HEK - 293细胞中表达了带有绿色荧光蛋白(GFP)标签的大鼠P2Y2(rP2Y2)受体,并通过共聚焦显微镜观察活细胞中的受体转位。通过测定[Ca2+]i反应来确认功能性受体的表达。激动剂刺激导致受体从质膜向细胞质发生时间依赖性转位。在激动剂介导的rP2Y2 - GFP受体内化过程中观察到肌动蛋白细胞骨架的重排。通过共聚焦显微镜检测到内化受体与早期内体、网格蛋白和溶酶体的共定位。在UTP存在的情况下,高密度培养基或氯丙嗪对受体内吞作用的抑制表明该受体是通过网格蛋白介导的途径内化的。小窝蛋白介导的途径未参与其中。受体从内体靶向溶酶体似乎涉及蛋白酶体途径,因为蛋白酶体抑制增加了受体回收到质膜的再循环。