List of Publications (2011-Current)
2022
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
Anoctamin 1/TMEM16A in pruritoceptors is essential for Mas-related G protein receptor–dependent itch Journal Article
In: PAIN, vol. 163, no. 11, pp. 2172–2184, 2022, ISSN: 1872-6623.
Abstract | Links | BibTeX | Tags: Anoctamin 1, Itch, MrgprA3, MrgprC11
@article{Kim2022,
title = {Anoctamin 1/TMEM16A in pruritoceptors is essential for Mas-related G protein receptor–dependent itch},
author = {Hyesu Kim and Hyungsup Kim and Hawon Cho and Byeongjun Lee and Huan-Jun Lu and Kyungmin Kim and Sooyoung Chung and Won-Sik Shim and Young Kee Shin and Xinzhong Dong and John N. Wood and Uhtaek Oh},
doi = {10.1097/j.pain.0000000000002611},
issn = {1872-6623},
year = {2022},
date = {2022-00-00},
urldate = {2022-00-00},
journal = {PAIN},
volume = {163},
number = {11},
pages = {2172--2184},
publisher = {Ovid Technologies (Wolters Kluwer Health)},
abstract = {<jats:title>Abstract</jats:title>
<jats:p>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 Ca<jats:sup>2+</jats:sup>-activated chloride channel, is a transduction channel mediating Mrgpr-dependent itch signals. Genetic ablation of <jats:italic toggle="yes">Ano1</jats:italic> 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 Ca<jats:sup>2+</jats:sup> imaging and electrophysiological recording revealed that chloroquine and other agonists of Mrgprs excited DRG neurons via ANO1. More importantly, the overexpression of <jats:italic toggle="yes">Ano1</jats:italic> in DRG neurons of <jats:italic toggle="yes">Ano1</jats:italic>-deficient mice rescued the impaired itching observed in <jats:italic toggle="yes">Ano1</jats:italic>-deficient mice. These results demonstrate that ANO1 mediates the Mrgpr-dependent itch signaling in pruriceptors and provides clues to treating pathologic itch syndromes.</jats:p>},
keywords = {Anoctamin 1, Itch, MrgprA3, MrgprC11},
pubstate = {published},
tppubtype = {article}
}
<jats:title>Abstract</jats:title>
<jats:p>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 Ca<jats:sup>2+</jats:sup>-activated chloride channel, is a transduction channel mediating Mrgpr-dependent itch signals. Genetic ablation of <jats:italic toggle="yes">Ano1</jats:italic> 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 Ca<jats:sup>2+</jats:sup> imaging and electrophysiological recording revealed that chloroquine and other agonists of Mrgprs excited DRG neurons via ANO1. More importantly, the overexpression of <jats:italic toggle="yes">Ano1</jats:italic> in DRG neurons of <jats:italic toggle="yes">Ano1</jats:italic>-deficient mice rescued the impaired itching observed in <jats:italic toggle="yes">Ano1</jats:italic>-deficient mice. These results demonstrate that ANO1 mediates the Mrgpr-dependent itch signaling in pruriceptors and provides clues to treating pathologic itch syndromes.</jats:p>
<jats:p>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 Ca<jats:sup>2+</jats:sup>-activated chloride channel, is a transduction channel mediating Mrgpr-dependent itch signals. Genetic ablation of <jats:italic toggle="yes">Ano1</jats:italic> 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 Ca<jats:sup>2+</jats:sup> imaging and electrophysiological recording revealed that chloroquine and other agonists of Mrgprs excited DRG neurons via ANO1. More importantly, the overexpression of <jats:italic toggle="yes">Ano1</jats:italic> in DRG neurons of <jats:italic toggle="yes">Ano1</jats:italic>-deficient mice rescued the impaired itching observed in <jats:italic toggle="yes">Ano1</jats:italic>-deficient mice. These results demonstrate that ANO1 mediates the Mrgpr-dependent itch signaling in pruriceptors and provides clues to treating pathologic itch syndromes.</jats:p>