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Angiotensin II‐Induced Golgi Translocation of the AT1 and AT2 Receptors

AT1 and AT2 receptors are G protein‐coupled seven transmembrane receptors. They bind Angiotensin II (Ang II), an octapeptide hormone, to regulate diverse physiological actions. Similar to most GPCRs, AT1 but not AT2 receptor expressed on the cell surface undergoes conventional endocytosis for degradation and recycling upon ligand activation. Interestingly, recent evidence shows that Ang II also induces nuclear translocation of the AT1 receptors. In HEK293 cells that stably express AT1 and AT2 receptors tagged with GFP at the C‐terminal or HA at the N‐terminal (AT1‐GFP, HA‐AT2‐GFP, HA‐AT1 and HA‐AT2), we observed Ang II‐induced perinuclear accumulation of the AT1 receptors under confocal laser scanning microscope. Surprisingly, Ang II also induced Golgi accumulation of both receptors as detected with Golgi‐specific dye BODPIY TR. Distinct from conventional endocytosis that results in about 50% AT1 receptor internalization within the first 15 min of Ang II stimulation, the Golgi accumulation occurred 30 min after the stimulation. With fluorescein‐labeled FITC‐Ang II, we found that FITC‐Ang II co‐localizes with AT1 and AT2 receptors in the Golgi. DRY/tL314, an AT1 mutant deficient in G protein activation and conventional internalization, underwent almost intact Golgi translocation, suggesting a novel endocytosis pathway. In conclusion, we have identified the Ang II‐induced translocation of AT1 and AT2 receptors from plasma membrane to Golgi. These results suggest an undefined function of Golgi in receptor endocytosis and/or an unidentified role of Ang II receptors in regulation of Golgi function.