Petrou C P, Tashjian A H
Department of Molecular and Cellular Toxicology, Harvard School of Public Health, Boston, MA.
Biochem J. 1995 Feb 15;306 ( Pt 1)(Pt 1):107-13. doi: 10.1042/bj3060107.
We have examined the trafficking of the thyrotropin-releasing hormone receptor (TRHR) and its ligand, after TRHR-TRH internalization in rat pituitary GH4C1 cells. After rapid ligand-induced receptor sequestration, the cell surface receptor pool was replenished. Replenishment was insensitive to inhibition of protein synthesis and was dependent on the duration of internalization; therefore, the replenished receptors were not newly synthesized but recycled. The total amount of recycled receptors decreased with increasing internalization time, resulting in only partial replenishment of the cell-surface receptor pool after prolonged incubation with ligand. Thus, in addition to a receptor recycling pathway, a non-cycling route exists for TRHR sorting; this route became dominant with increasing internalization periods. TRHR entry into these pathways was not determined by the affinity of the receptor-ligand interaction, because the extent of receptor recycling was similar after TRH- and methyl-TRH (MeTRH)-induced internalization. Unlike results with the TRHR, the TRH recycling pool was not depleted by the noncycling pathway. After multiple rounds of [3H]MeTRH internalization, the amount of cell-associated radioactivity increased with increasing internalization time due to accumulation of the ligand or its metabolites in a non-cycling pathway, but the absolute amount of recycled ligand remained constant after short or long internalization times. The difference in the proportion of TRHR and MeTRH that were diverted into a noncycling pathway indicated intracellular dissociation of the internalized TRHR-TRH complex. Dissociation of the internalized TRHR-TRH complex was dependent on the acidic pH in an intracellular compartment. Although extracellular acidic pH did not enhance cell-surface receptor-ligand (RL) dissociation, bafilomycin A1 inhibited both receptor and ligand recycling. We conclude that the TRHR-TRH system is unique among recycling receptors because, after RL sequestration, the TRHR-TRH complex becomes dissociated intracellularly via a bafilomycin A1-sensitive, acidic pH-dependent mechanism, and both the unoccupied TRHR and TRH recycle disassociated from each other.
我们研究了大鼠垂体GH4C1细胞中促甲状腺激素释放激素受体(TRHR)及其配体在TRHR - TRH内化后的运输情况。在配体诱导受体快速隔离后,细胞表面受体库得到补充。这种补充对蛋白质合成抑制不敏感,且依赖于内化的持续时间;因此,补充的受体不是新合成的,而是循环利用的。随着内化时间的增加,循环受体的总量减少,导致在与配体长时间孵育后,细胞表面受体库仅得到部分补充。因此,除了受体循环途径外,TRHR分选还存在一条非循环途径;随着内化时间的增加,这条途径变得占主导地位。TRHR进入这些途径并非由受体 - 配体相互作用的亲和力决定,因为TRH和甲基 - TRH(MeTRH)诱导内化后受体循环的程度相似。与TRHR的结果不同,TRH的循环库并未因非循环途径而耗尽。经过多轮[3H]MeTRH内化后,由于配体或其代谢产物在非循环途径中的积累,细胞相关放射性的量随着内化时间的增加而增加,但内化时间短或长时,循环配体的绝对量保持恒定。TRHR和MeTRH进入非循环途径的比例差异表明内化的TRHR - TRH复合物在细胞内发生了解离。内化的TRHR - TRH复合物的解离依赖于细胞内区室的酸性pH。虽然细胞外酸性pH不会增强细胞表面受体 - 配体(RL)的解离,但巴弗洛霉素A1抑制受体和配体的循环。我们得出结论,TRHR - TRH系统在循环受体中是独特的,因为在RL隔离后,TRHR - TRH复合物通过巴弗洛霉素A1敏感的、酸性pH依赖的机制在细胞内解离,未占据的TRHR和TRH彼此解离后循环利用。