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- W4210809802 abstract "Abstract Efficacy of monoclonal antibodies against calcitonin gene-related peptide (CGRP) or its receptor (calcitonin receptor-like receptor/receptor activity modifying protein-1, CLR/RAMP1) implicates peripherally-released CGRP in migraine pain. However, the site and mechanism of CGRP-evoked peripheral pain remain unclear. By cell-selective RAMP1 gene deletion, we reveal that CGRP released from mouse cutaneous trigeminal fibers targets CLR/RAMP1 on surrounding Schwann cells to evoke periorbital mechanical allodynia. CLR/RAMP1 activation in human and mouse Schwann cells generates long-lasting signals from endosomes that evoke cAMP-dependent formation of NO. NO, by gating Schwann cell transient receptor potential ankyrin 1 (TRPA1), releases ROS, which in a feed-forward manner sustain allodynia via nociceptor TRPA1. When encapsulated into nanoparticles that release cargo in acidified endosomes, a CLR/RAMP1 antagonist provides superior inhibition of CGRP signaling and allodynia in mice. Our data suggest that the CGRP-mediated neuronal/Schwann cell pathway mediates allodynia associated with neurogenic inflammation, contributing to the algesic action of CGRP in mice." @default.
- W4210809802 created "2022-02-08" @default.
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- W4210809802 date "2022-02-03" @default.
- W4210809802 modified "2023-10-06" @default.
- W4210809802 title "Schwann cell endosome CGRP signals elicit periorbital mechanical allodynia in mice" @default.
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- W4210809802 doi "https://doi.org/10.1038/s41467-022-28204-z" @default.
- W4210809802 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35115501" @default.
- W4210809802 hasPublicationYear "2022" @default.
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