| Literature DB >> 28223516 |
Zhe Li1, Pang-Yen Tseng1, Vinod Tiwari2, Qian Xu1, Shao-Qiu He2, Yan Wang1, Qin Zheng1, Liang Han1, Zhiping Wu3,4, Anna L Blobaum5, Yiyuan Cui6, Vineeta Tiwari2, Shuohao Sun1, Yingying Cheng1, Julie H Y Huang-Lionnet2, Yixun Geng1, Bo Xiao6, Junmin Peng3,4,7, Corey Hopkins5, Srinivasa N Raja2, Yun Guan8, Xinzhong Dong9,10.
Abstract
Human Mas-related G protein-coupled receptor X1 (MRGPRX1) is a promising target for pain inhibition, mainly because of its restricted expression in nociceptors within the peripheral nervous system. However, constrained by species differences across Mrgprs, drug candidates that activate MRGPRX1 do not activate rodent receptors, leaving no responsive animal model to test the effect on pain in vivo. Here, we generated a transgenic mouse line in which we replaced mouse Mrgprs with human MrgprX1 This humanized mouse allowed us to characterize an agonist [bovine adrenal medulla 8-22 (BAM8-22)] and a positive allosteric modulator (PAM), ML382, of MRGPRX1. Cellular studies suggested that ML382 enhances the ability of BAM8-22 to inhibit high-voltage-activated Ca2+ channels and attenuate spinal nociceptive transmission. Importantly, both BAM8-22 and ML382 effectively attenuated evoked, persistent, and spontaneous pain without causing obvious side effects. Notably, ML382 by itself attenuated both evoked pain hypersensitivity and spontaneous pain in MrgprX1 mice after nerve injury without acquiring coadministration of an exogenous agonist. Our findings suggest that humanized MrgprX1 mice provide a promising preclinical model and that activating MRGPRX1 is an effective way to treat persistent pain.Entities:
Keywords: DRG neurons; GPCR; MrgprX1; pain; positive allosteric modulator
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Year: 2017 PMID: 28223516 PMCID: PMC5347560 DOI: 10.1073/pnas.1615255114
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN: 0027-8424 Impact factor: 11.205