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

Angiotensin II type 1 receptor (AT1R)-mediated acute catecholamine release is modulated by β-arrestin. Here the authors show that β-arrestin-1 recruits the Ca2+channel TRPC3 and the PLCγ to the AT1R-β-arrestin complex, triggering G protein-independent calcium influx and catecholamine secretion.

Bibliographic Details
Main Authors: 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, Jin-Peng Sun
Format: Article
Language:English
Published: Nature Publishing Group 2017-02-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/ncomms14335
id doaj-fd8251bd4bfc4bada3441c9bdef9e02e
record_format Article
spelling doaj-fd8251bd4bfc4bada3441c9bdef9e02e2021-05-11T07:19:29ZengNature Publishing GroupNature Communications2041-17232017-02-018111710.1038/ncomms14335Arrestin-biased AT1R agonism induces acute catecholamine secretion through TRPC3 couplingChun-Hua Liu0Zheng Gong1Zong-Lai Liang2Zhi-Xin Liu3Fan Yang4Yu-Jing Sun5Ming-Liang Ma6Yi-Jing Wang7Chao-Ran Ji8Yu-Hong Wang9Mei-Jie Wang10Fu-Ai Cui11Amy Lin12Wen-Shuai Zheng13Dong-Fang He14Chang-xiu Qu15Peng Xiao16Chuan-Yong Liu17Alex R. B. Thomsen18Thomas Joseph Cahill19Alem W. Kahsai20Fan Yi21Kun-Hong Xiao22Tian Xue23Zhuan Zhou24Xiao Yu25Jin-Peng Sun26Department of Biochemistry and Molecular Biology, Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of MedicineDepartment of Biochemistry and Molecular Biology, Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of MedicineDepartment of Physiology, Shandong University School of MedicineDepartment of Biochemistry and Molecular Biology, Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of MedicineDepartment of Physiology, Shandong University School of MedicineDepartment of Biochemistry and Molecular Biology, Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of MedicineDepartment of Biochemistry and Molecular Biology, Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of MedicineDepartment of Biochemistry and Molecular Biology, Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of MedicineDepartment of Physiology, Shandong University School of MedicineDepartment of Biochemistry and Molecular Biology, Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of MedicineDepartment of Biochemistry and Molecular Biology, Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of MedicineDepartment of Biochemistry and Molecular Biology, Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of MedicineDuke University, School of MedicineDepartment of Physiology, Shandong University School of MedicineDepartment of Biochemistry and Molecular Biology, Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of MedicineDepartment of Biochemistry and Molecular Biology, Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of MedicineDepartment of Biochemistry and Molecular Biology, Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of MedicineDepartment of Physiology, Shandong University School of MedicineDuke University, School of MedicineDuke University, School of MedicineDuke University, School of MedicineDepartment of Pharmacology, Shandong University School of MedicineDuke University, School of MedicineHefei National Laboratory for Physical Science at Microscale, School of Life Science, University of Science and Technology of ChinaLaboratory of Cellular Biophysics and Neurodegeneration, Ying-Jie Conference Center, Peking UniversityDepartment of Physiology, Shandong University School of MedicineDepartment of Biochemistry and Molecular Biology, Key Laboratory Experimental Teratology of the Ministry of Education, Shandong University School of MedicineAngiotensin II type 1 receptor (AT1R)-mediated acute catecholamine release is modulated by β-arrestin. Here the authors show that β-arrestin-1 recruits the Ca2+channel TRPC3 and the PLCγ to the AT1R-β-arrestin complex, triggering G protein-independent calcium influx and catecholamine secretion.https://doi.org/10.1038/ncomms14335
collection DOAJ
language English
format Article
sources DOAJ
author 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
Jin-Peng Sun
spellingShingle 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
Jin-Peng Sun
Arrestin-biased AT1R agonism induces acute catecholamine secretion through TRPC3 coupling
Nature Communications
author_facet 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
Jin-Peng Sun
author_sort Chun-Hua Liu
title Arrestin-biased AT1R agonism induces acute catecholamine secretion through TRPC3 coupling
title_short Arrestin-biased AT1R agonism induces acute catecholamine secretion through TRPC3 coupling
title_full Arrestin-biased AT1R agonism induces acute catecholamine secretion through TRPC3 coupling
title_fullStr Arrestin-biased AT1R agonism induces acute catecholamine secretion through TRPC3 coupling
title_full_unstemmed Arrestin-biased AT1R agonism induces acute catecholamine secretion through TRPC3 coupling
title_sort arrestin-biased at1r agonism induces acute catecholamine secretion through trpc3 coupling
publisher Nature Publishing Group
series Nature Communications
issn 2041-1723
publishDate 2017-02-01
description Angiotensin II type 1 receptor (AT1R)-mediated acute catecholamine release is modulated by β-arrestin. Here the authors show that β-arrestin-1 recruits the Ca2+channel TRPC3 and the PLCγ to the AT1R-β-arrestin complex, triggering G protein-independent calcium influx and catecholamine secretion.
url https://doi.org/10.1038/ncomms14335
work_keys_str_mv AT chunhualiu arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT zhenggong arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT zonglailiang arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT zhixinliu arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT fanyang arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT yujingsun arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT mingliangma arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT yijingwang arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT chaoranji arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT yuhongwang arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT meijiewang arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT fuaicui arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT amylin arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT wenshuaizheng arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT dongfanghe arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT changxiuqu arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT pengxiao arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT chuanyongliu arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT alexrbthomsen arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT thomasjosephcahill arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT alemwkahsai arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT fanyi arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT kunhongxiao arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT tianxue arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT zhuanzhou arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT xiaoyu arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
AT jinpengsun arrestinbiasedat1ragonisminducesacutecatecholaminesecretionthroughtrpc3coupling
_version_ 1721452533671526400