ArticleFrontiers in pharmacology2020
Interplay Between Angiotensin II Type 1 Receptor and Thrombin Receptor Revealed by Bioluminescence Resonance Energy Transfer Assay.
Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Gating Mechanism for Biased Agonism at Angiotensin II Type 1 Receptors.Molecules (Basel, Switzerland) · 2025Article
- Advances in the allostery of angiotensin II type 1 receptor.Cell & bioscience · 2023Review
- Review
- Role of G-Proteins and GPCRs in Cardiovascular Pathologies.Bioengineering (Basel, Switzerland) · 2023Review
- Profiling novel pharmacology of receptor complexes using Receptor-HIT.Biochemical Society transactions · 2021Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The key hormone of the renin-angiotensin system (RAS), angiotensin II (AngII), and thrombin are known to play major roles in the vascular system and its related disorders. Previous studies reported connections between AngII and thrombin in both physiological and pathophysiological models. However, the molecular mechanisms controlling such interplay at the level of their receptors belonging to the family of G protein-coupled receptors (GPCRs) are not fully understood. In this study, we investigated the functional interaction between the AngII type 1 receptor (AT1R) and the thrombin receptor [or protease-activated receptor 1 (PAR1)] in human embryonic kidney 293 (HEK293) cells. For this, we used various bioluminescence resonance energy transfer (BRET) proximity-based assays to profile the coupling to the heterotrimeric Gαq protein, β-arrestin recruitment, and receptor internalization and trafficking in intact cells. The overall dose-response and real-time kinetic BRET data demonstrated the specific molecular proximity between AT1R and PAR1 resulting in their functional interaction. This was characterized by thrombin inducing BRET increase within AT1R/Gαq and AT1R/β-arrestin pairs and synergistic effects observed upon the concomitant activation of both receptors suggesting a positive allosteric interaction. The BRET data corroborated with the data on the downstream Gαq/inositol phosphate pathway. Moreover, the selective pharmacological blockade of the receptors revealed the implication of both AT1R and PAR1 protomers in such a synergistic interaction and the possible transactivation of AT1R by PAR1. Interestingly, the positive action of PAR1 on AT1R activation was contrasted with its apparent inhibition of AT1R internalization and its endosomal trafficking. Finally, BRET saturation and co-immunoprecipitation assays supported the physical AT1-PAR1 interaction in HEK293 cells. Our study reveals for the first time the functional interaction between AT1R and PAR1
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