Arrestin-biased AT1R agonism induces acute catecholamine secretion through TRPC3 coupling

Chun-Hua Liu, Zheng Gong, Zong-Lai Liang, Zhi-Xin Liu, Fan Yang, Yu-Jing Sun, Ming-Liang Ma, Yi-Jing Wang, Chao-Ran Ji, Yu-Hong Wang, Mei-Jie Wang, Fu-Ai Cui, Amy Lin, Wen-Shuai Zheng, Dong-Fang He, Chang-xiu Qu, Peng Xiao, Chuan-Yong Liu, Alex R. B. Thomsen, Thomas Joseph Cahill, Alem W. Kahsai, Fan Yi, Kun-Hong Xiao, Tian Xue, Zhuan Zhou, Xiao Yu and Jin-Peng Sun ()
Additional contact information
Chun-Hua Liu: Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of Medicine
Zheng Gong: Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of Medicine
Zong-Lai Liang: Shandong University School of Medicine
Zhi-Xin Liu: Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of Medicine
Fan Yang: Shandong University School of Medicine
Yu-Jing Sun: Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of Medicine
Ming-Liang Ma: Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of Medicine
Yi-Jing Wang: Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of Medicine
Chao-Ran Ji: Shandong University School of Medicine
Yu-Hong Wang: Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of Medicine
Mei-Jie Wang: Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of Medicine
Fu-Ai Cui: Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of Medicine
Amy Lin: Duke University, School of Medicine
Wen-Shuai Zheng: Shandong University School of Medicine
Dong-Fang He: Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of Medicine
Chang-xiu Qu: Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of Medicine
Peng Xiao: Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of Medicine
Chuan-Yong Liu: Shandong University School of Medicine
Alex R. B. Thomsen: Duke University, School of Medicine
Thomas Joseph Cahill: Duke University, School of Medicine
Alem W. Kahsai: Duke University, School of Medicine
Fan Yi: Shandong University School of Medicine
Kun-Hong Xiao: Duke University, School of Medicine
Tian Xue: Hefei National Laboratory for Physical Science at Microscale, School of Life Science, University of Science and Technology of China
Zhuan Zhou: Laboratory of Cellular Biophysics and Neurodegeneration, Ying-Jie Conference Center, Peking University
Xiao Yu: Shandong University School of Medicine
Jin-Peng Sun: Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of Medicine

Nature Communications, 2017, vol. 8, issue 1, 1-17

Abstract: Abstract Acute hormone secretion triggered by G protein-coupled receptor (GPCR) activation underlies many fundamental physiological processes. GPCR signalling is negatively regulated by β-arrestins, adaptor molecules that also activate different intracellular signalling pathways. Here we reveal that TRV120027, a β-arrestin-1-biased agonist of the angiotensin II receptor type 1 (AT1R), stimulates acute catecholamine secretion through coupling with the transient receptor potential cation channel subfamily C 3 (TRPC3). We show that TRV120027 promotes the recruitment of TRPC3 or phosphoinositide-specific phospholipase C (PLCγ) to the AT1R-β-arrestin-1 signalling complex. Replacing the C-terminal region of β-arrestin-1 with its counterpart on β-arrestin-2 or using a specific TAT-P1 peptide to block the interaction between β-arrestin-1 and PLCγ abolishes TRV120027-induced TRPC3 activation. Taken together, our results show that the GPCR-arrestin complex initiates non-desensitized signalling at the plasma membrane by coupling with ion channels. This fast communication pathway might be a common mechanism of several cellular processes.

Date: 2017
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DOI: 10.1038/ncomms14335

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