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Role of ERK1/2 activation on itch sensation induced by bradykinin B1 activation in inflamed skin

It has previously been demonstrated that bradykinin receptor B1 (B1R) agonists evoke an itch-related scratching response in inflamed skin via the B1 receptor; however, the mechanisms responsible for this abnormal itch sensation remain unclear. Therefore, the present study utilized a complete Freund&...

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Autores principales: Chen, Yuanzhen, Jiang, Shuyan, Liu, Yuying, Xiong, Jialing, Liang, Jiexian, Ji, Wenjin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4950635/
https://www.ncbi.nlm.nih.gov/pubmed/27446253
http://dx.doi.org/10.3892/etm.2016.3426
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author Chen, Yuanzhen
Jiang, Shuyan
Liu, Yuying
Xiong, Jialing
Liang, Jiexian
Ji, Wenjin
author_facet Chen, Yuanzhen
Jiang, Shuyan
Liu, Yuying
Xiong, Jialing
Liang, Jiexian
Ji, Wenjin
author_sort Chen, Yuanzhen
collection PubMed
description It has previously been demonstrated that bradykinin receptor B1 (B1R) agonists evoke an itch-related scratching response in inflamed skin via the B1 receptor; however, the mechanisms responsible for this abnormal itch sensation remain unclear. Therefore, the present study utilized a complete Freund's adjuvant (CFA)-induced mouse model of inflammation to elucidate the mechanisms responsible. Over a period of 30 min, scratching behavior was quantified by the number of hind limb scratches of the area surrounding the drug injection site on the neck. Furthermore, western blot analysis was used to investigate the potential role of extracellular signal-regulated kinase (ERK) 1/2 signaling as a mediator of itch in CFA-treated mice. The results demonstrated that CFA-induced inflammation at the back of the neck is associated with sustained enhancement of ERK1/2 activation in the spinal cord. Moreover, B1R agonist treatment resulted in increased expression of phosphorylated ERK1/2 in the spinal cord, which peaked at 45 min. Consistent with these findings, inhibition of either mitogen-activated protein/ERK kinase or ERK1/2, as well as inhibition of ERK1/2 activation following inflammation, attenuated B1 receptor-mediated scratching responses to a greater extent, as compared with control mice. Collectively, the results of the present study indicated that enhanced and persistent ERK1/2 activation in the spinal cord may be required to induce a scratching response to B1R agonists following CFA-induced inflammation.
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spelling pubmed-49506352016-07-21 Role of ERK1/2 activation on itch sensation induced by bradykinin B1 activation in inflamed skin Chen, Yuanzhen Jiang, Shuyan Liu, Yuying Xiong, Jialing Liang, Jiexian Ji, Wenjin Exp Ther Med Articles It has previously been demonstrated that bradykinin receptor B1 (B1R) agonists evoke an itch-related scratching response in inflamed skin via the B1 receptor; however, the mechanisms responsible for this abnormal itch sensation remain unclear. Therefore, the present study utilized a complete Freund's adjuvant (CFA)-induced mouse model of inflammation to elucidate the mechanisms responsible. Over a period of 30 min, scratching behavior was quantified by the number of hind limb scratches of the area surrounding the drug injection site on the neck. Furthermore, western blot analysis was used to investigate the potential role of extracellular signal-regulated kinase (ERK) 1/2 signaling as a mediator of itch in CFA-treated mice. The results demonstrated that CFA-induced inflammation at the back of the neck is associated with sustained enhancement of ERK1/2 activation in the spinal cord. Moreover, B1R agonist treatment resulted in increased expression of phosphorylated ERK1/2 in the spinal cord, which peaked at 45 min. Consistent with these findings, inhibition of either mitogen-activated protein/ERK kinase or ERK1/2, as well as inhibition of ERK1/2 activation following inflammation, attenuated B1 receptor-mediated scratching responses to a greater extent, as compared with control mice. Collectively, the results of the present study indicated that enhanced and persistent ERK1/2 activation in the spinal cord may be required to induce a scratching response to B1R agonists following CFA-induced inflammation. D.A. Spandidos 2016-08 2016-06-06 /pmc/articles/PMC4950635/ /pubmed/27446253 http://dx.doi.org/10.3892/etm.2016.3426 Text en Copyright: © Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Chen, Yuanzhen
Jiang, Shuyan
Liu, Yuying
Xiong, Jialing
Liang, Jiexian
Ji, Wenjin
Role of ERK1/2 activation on itch sensation induced by bradykinin B1 activation in inflamed skin
title Role of ERK1/2 activation on itch sensation induced by bradykinin B1 activation in inflamed skin
title_full Role of ERK1/2 activation on itch sensation induced by bradykinin B1 activation in inflamed skin
title_fullStr Role of ERK1/2 activation on itch sensation induced by bradykinin B1 activation in inflamed skin
title_full_unstemmed Role of ERK1/2 activation on itch sensation induced by bradykinin B1 activation in inflamed skin
title_short Role of ERK1/2 activation on itch sensation induced by bradykinin B1 activation in inflamed skin
title_sort role of erk1/2 activation on itch sensation induced by bradykinin b1 activation in inflamed skin
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4950635/
https://www.ncbi.nlm.nih.gov/pubmed/27446253
http://dx.doi.org/10.3892/etm.2016.3426
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