Anoctamin 1/TMEM16A in pruritoceptors is essential for Mas-related G protein receptor-dependent itch
- Authors
- Kim, Hyesu; Kim, Hyungsup; Cho, Hawon; Lee, Byeongjun; Lu, Huan-Jun; Kim, Kyungmin; Chung, Sooyoung; Shim, Won-Sik; Shin, Young Kee; Dong, Xinzhong; Wood, John N.; Oh, Uhtaek
- Issue Date
- Nov-2022
- Publisher
- LIPPINCOTT WILLIAMS & WILKINS
- Keywords
- Anoctamin 1; Pruriceptors; Itch; Mrgprs; Bilirubin; Chloroquine
- Citation
- PAIN, v.163, no.11, pp.2172 - 2184
- Journal Title
- PAIN
- Volume
- 163
- Number
- 11
- Start Page
- 2172
- End Page
- 2184
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/85986
- DOI
- 10.1097/j.pain.0000000000002611
- ISSN
- 0304-3959
- Abstract
- Itch is an unpleasant sensation that evokes a desire to scratch. Pathologic conditions such as allergy or atopic dermatitis produce severe itching sensation. Mas-related G protein receptors (Mrgprs) are receptors for many endogenous pruritogens. However, signaling pathways downstream to these receptors in dorsal root ganglion (DRG) neurons are not yet understood. We found that anoctamin 1 (ANO1), a Ca2+-activated chloride channel, is a transduction channel mediating Mrgpr-dependent itch signals. Genetic ablation of Ano1 in DRG neurons displayed a significant reduction in scratching behaviors in response to acute and chronic Mrgpr-dependent itch models and the epidermal hyperplasia induced by dry skin. In vivo Ca2+ imaging and electrophysiological recording revealed that chloroquine and other agonists of Mrgprs excited DRG neurons via ANO1. More importantly, the overexpression of Ano1 in DRG neurons of Ano1-deficient mice rescued the impaired itching observed in Ano1-deficient mice. These results demonstrate that ANO1 mediates the Mrgpr-dependent itch signaling in pruriceptors and provides clues to treating pathologic itch syndromes.
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