ArticleCell research2021
Cartilage oligomeric matrix protein is an endogenous β-arrestin-2-selective allosteric modulator of AT1 receptor counteracting vascular injury.
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Article in Cell research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 58 citations in OpenAlex.
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- The molecular mechanism of thrombospondin family members in cardiovascular diseases.Frontiers in cardiovascular medicine · 2024Review
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- COMP Improves Ang-II-Induced Atrial Fibrillation via TGF-β Signaling Pathway.Cardiovascular toxicology · 2023Article
- Orthosteric ligand selectivity and allosteric probe dependence at Hydroxycarboxylic acid receptor HCAR2.Signal transduction and targeted therapy · 2023Article
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- Single hormone or synthetic agonist induces GProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Advances in the allostery of angiotensin II type 1 receptor.Cell & bioscience · 2023Review
- Deafness-Associated ADGRV1 Mutation Impairs USH2A Stability through Improper Phosphorylation of WHRN and WDSUB1 Recruitment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
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Authors and funding
33 authors at 7 institutions in 3 countries.
Yi Fu *Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Yaqian Huang *Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Zhao Yang *Department of Biochemistry & Molecular Biology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.
Yufei ChenDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Jingang ZhengDepartment of Cardiology, China-Japan Friendship Hospital, Beijing, 100029, China.
Chenfeng MaoDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Zhiqing LiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Zhixin LiuDepartment of Biochemistry & Molecular Biology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.
Bing YuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Tuoyi LiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Meili WangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Chanjuan XuCollege of Life Science and Technology, Collaborative Innovation Center for Brain Science, Huazhong University of Science and Technology; Key Laboratory of Molecular Biophysics, Ministry of Education, Wuhan, Hubei, 430074, China.
Yiwei ZhouCollege of Life Science and Technology, Collaborative Innovation Center for Brain Science, Huazhong University of Science and Technology; Key Laboratory of Molecular Biophysics, Ministry of Education, Wuhan, Hubei, 430074, China.
Guizhen ZhaoDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Yiting JiaDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Wei GuoDepartment of Vascular Surgery, Chinese PLA General Hospital, Beijing, 100853, China.
Xin JiaDepartment of Vascular Surgery, Chinese PLA General Hospital, Beijing, 100853, China.
Tao ZhangDepartment of Vascular Surgery, Chinese PLA General Hospital, Beijing, 100853, China.
Li LiDepartment of Pathology, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100037, China.
Ziyi LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Shengchao GuoDepartment of Biochemistry & Molecular Biology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.
Mingliang MaDepartment of Biochemistry & Molecular Biology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.
Heng ZhangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Bo LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Junbao DuDepartment of Pediatrics, Peking University First Hospital, Beijing, 100034, China.
Wengong WangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.ORCID http://orcid.org/0000-0002-1720-809X
Chaoshu TangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Pei GaoDepartment of Epidemiology and Biostatistics, School of Public Health, Peking University Health Science Center, Beijing, 100191, China.
Qingbo XuCardiovascular Division, The James Black Centre, King's College London, London, SE5 9NU, UK.
Xian WangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
Jianfeng LiuCollege of Life Science and Technology, Collaborative Innovation Center for Brain Science, Huazhong University of Science and Technology; Key Laboratory of Molecular Biophysics, Ministry of Education, Wuhan, Hubei, 430074, China.ORCID http://orcid.org/0000-0002-0284-8377
Jinpeng SunDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China. sunjinpeng@sdu.edu.cn.
Wei KongDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China. kongw@bjmu.edu.cn.
Ministry of Education of the People's Republic of China · CNShandong University · CNChinese PLA General Hospital · CNHuazhong University of Science and Technology · CNPeking University · CNChina-Japan Friendship Hospital · CNKing's College London · GB
Funding
No grant is acknowledged in the PubMed record.
Abstract
Compelling evidence has revealed that biased activation of G protein-coupled receptor (GPCR) signaling, including angiotensin II (AngII) receptor type 1 (AT1) signaling, plays pivotal roles in vascular homeostasis and injury, but whether a clinically relevant endogenous biased antagonism of AT1 signaling exists under physiological and pathophysiological conditions has not been clearly elucidated. Here, we show that an extracellular matrix protein, cartilage oligomeric matrix protein (COMP), acts as an endogenous allosteric biased modulator of the AT1 receptor and its deficiency is clinically associated with abdominal aortic aneurysm (AAA) development. COMP directly interacts with the extracellular N-terminus of the AT1 via its EGF domain and inhibits AT1-β-arrestin-2 signaling, but not Gq or Gi signaling, in a selective manner through allosteric regulation of AT1 intracellular conformational states. COMP deficiency results in activation of AT1a-β-arrestin-2 signaling and subsequent exclusive AAA formation in response to AngII infusion. AAAs in COMP
Indexed as
Receptor, Angiotensin, Type 1Vascular System InjuriesAnimalsbeta-Arrestin 2beta-ArrestinsCartilage Oligomeric Matrix ProteinHEK293 CellsHumansMicebeta-Arrestin 2beta-ArrestinsCartilage Oligomeric Matrix ProteinReceptor, Angiotensin, Type 1
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