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Involvement of Endoplasmic Reticulum Stress Response in Orofacial Inflammatory Pain
Endoplasmic reticulum (ER) stress is involved in many neurological diseases and inflammatory responses. Inflammatory mediators induce neuronal damage and trigger the neuropathic or inflammatory pain. But there is very little data on the role of the ER stress response in pain mechanisms. In this stud...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Society for Brain and Neural Science
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4276808/ https://www.ncbi.nlm.nih.gov/pubmed/25548537 http://dx.doi.org/10.5607/en.2014.23.4.372 |
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author | Yang, Eun Sun Bae, Jin Young Kim, Tae Heon Kim, Yun Sook Suk, Kyoungho Bae, Yong Chul |
author_facet | Yang, Eun Sun Bae, Jin Young Kim, Tae Heon Kim, Yun Sook Suk, Kyoungho Bae, Yong Chul |
author_sort | Yang, Eun Sun |
collection | PubMed |
description | Endoplasmic reticulum (ER) stress is involved in many neurological diseases and inflammatory responses. Inflammatory mediators induce neuronal damage and trigger the neuropathic or inflammatory pain. But there is very little data on the role of the ER stress response in pain mechanisms. In this study, we explored whether the ER stress response is involved in orofacial inflammatory pain by using a complete Freund's adjuvant (CFA)-injected rat model. The thermal pain hypersensitivity increased significantly after CFA injection. We found that the protein and mRNA levels of ER stress response genes, GRP78/Bip and p-eIF2α, increased significantly in trigeminal ganglion (TG) of CFA-injected rats compared to control animals. In immunofluorescence analysis, a significant increase of GRP78 and p-eIF2α immunopositive neurons was observed in CFA-injected TG compared to control TG. When we administered an ER stress modulator, salubrinal, CFA-induced thermal pain hypersensitivity was temporally reduced. Thus, our study suggests that ER stress responses in TG neurons contribute to CFA-induced inflammatory pain, and may comprise an important molecular mechanism underlying the orofacial inflammatory pain pathway. |
format | Online Article Text |
id | pubmed-4276808 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | The Korean Society for Brain and Neural Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-42768082014-12-29 Involvement of Endoplasmic Reticulum Stress Response in Orofacial Inflammatory Pain Yang, Eun Sun Bae, Jin Young Kim, Tae Heon Kim, Yun Sook Suk, Kyoungho Bae, Yong Chul Exp Neurobiol Original Article Endoplasmic reticulum (ER) stress is involved in many neurological diseases and inflammatory responses. Inflammatory mediators induce neuronal damage and trigger the neuropathic or inflammatory pain. But there is very little data on the role of the ER stress response in pain mechanisms. In this study, we explored whether the ER stress response is involved in orofacial inflammatory pain by using a complete Freund's adjuvant (CFA)-injected rat model. The thermal pain hypersensitivity increased significantly after CFA injection. We found that the protein and mRNA levels of ER stress response genes, GRP78/Bip and p-eIF2α, increased significantly in trigeminal ganglion (TG) of CFA-injected rats compared to control animals. In immunofluorescence analysis, a significant increase of GRP78 and p-eIF2α immunopositive neurons was observed in CFA-injected TG compared to control TG. When we administered an ER stress modulator, salubrinal, CFA-induced thermal pain hypersensitivity was temporally reduced. Thus, our study suggests that ER stress responses in TG neurons contribute to CFA-induced inflammatory pain, and may comprise an important molecular mechanism underlying the orofacial inflammatory pain pathway. The Korean Society for Brain and Neural Science 2014-12 2014-12-12 /pmc/articles/PMC4276808/ /pubmed/25548537 http://dx.doi.org/10.5607/en.2014.23.4.372 Text en Copyright © Experimental Neurobiology 2014. http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Yang, Eun Sun Bae, Jin Young Kim, Tae Heon Kim, Yun Sook Suk, Kyoungho Bae, Yong Chul Involvement of Endoplasmic Reticulum Stress Response in Orofacial Inflammatory Pain |
title | Involvement of Endoplasmic Reticulum Stress Response in Orofacial Inflammatory Pain |
title_full | Involvement of Endoplasmic Reticulum Stress Response in Orofacial Inflammatory Pain |
title_fullStr | Involvement of Endoplasmic Reticulum Stress Response in Orofacial Inflammatory Pain |
title_full_unstemmed | Involvement of Endoplasmic Reticulum Stress Response in Orofacial Inflammatory Pain |
title_short | Involvement of Endoplasmic Reticulum Stress Response in Orofacial Inflammatory Pain |
title_sort | involvement of endoplasmic reticulum stress response in orofacial inflammatory pain |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4276808/ https://www.ncbi.nlm.nih.gov/pubmed/25548537 http://dx.doi.org/10.5607/en.2014.23.4.372 |
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