Cargando…
Role of p120 Catenin in Epac1-Induced Chronic Postsurgical Pain in Rats
Chronic postsurgical pain (CPSP) is a chronic pain state that is difficult to be treated clinically. A series of complicated changes have been produced from nociceptive stimulation to the occurrence and development of postsurgical pain. Many mechanisms remain unclear. In order to study the role of i...
Autores principales: | , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2019
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6377980/ https://www.ncbi.nlm.nih.gov/pubmed/30863475 http://dx.doi.org/10.1155/2019/9017931 |
_version_ | 1783395838120165376 |
---|---|
author | Pan, Peng Huang, Sai-Sai Shen, Shi-Ren Lu, Cui-E. Qin, Yi-Bin Zhang, Jia-Long Cao, Su |
author_facet | Pan, Peng Huang, Sai-Sai Shen, Shi-Ren Lu, Cui-E. Qin, Yi-Bin Zhang, Jia-Long Cao, Su |
author_sort | Pan, Peng |
collection | PubMed |
description | Chronic postsurgical pain (CPSP) is a chronic pain state that is difficult to be treated clinically. A series of complicated changes have been produced from nociceptive stimulation to the occurrence and development of postsurgical pain. Many mechanisms remain unclear. In order to study the role of intercellular gap junctions in inducing inflammatory microenvironment at the beginning of nociceptor after operation, the model of skin/muscle incision and retraction (SMIR) was established. We observed the changes of the expression of exchange proteins directly activated by cAMP-1 (Epac1) and p120 catenin (p120), the quantities of macrophages and endothelial cells, vascular endothelial permeability, and mechanical withdrawal threshold (MWT). It was found that macrophages and endothelial cells were functionally coupled through Epac1-p120. Adhesive linkage disorder remodeled the chronic, inflammatory, and eutrophic microenvironment at the beginning of nociceptor after operation through macrophages, endothelial cells, and endothelial paracellular pathways. It might be an early event and a key step in peripheral sensitization of CPSP. The expression of p120 in muscle tissue around the incision might become a prognostic marker for the conversion of acute postsurgical pain into CPSP. Targeted intervention of Epac1-p120 might be a clinical strategy for inhibiting the conversion of acute postsurgical pain into CPSP. |
format | Online Article Text |
id | pubmed-6377980 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-63779802019-03-12 Role of p120 Catenin in Epac1-Induced Chronic Postsurgical Pain in Rats Pan, Peng Huang, Sai-Sai Shen, Shi-Ren Lu, Cui-E. Qin, Yi-Bin Zhang, Jia-Long Cao, Su Pain Res Manag Research Article Chronic postsurgical pain (CPSP) is a chronic pain state that is difficult to be treated clinically. A series of complicated changes have been produced from nociceptive stimulation to the occurrence and development of postsurgical pain. Many mechanisms remain unclear. In order to study the role of intercellular gap junctions in inducing inflammatory microenvironment at the beginning of nociceptor after operation, the model of skin/muscle incision and retraction (SMIR) was established. We observed the changes of the expression of exchange proteins directly activated by cAMP-1 (Epac1) and p120 catenin (p120), the quantities of macrophages and endothelial cells, vascular endothelial permeability, and mechanical withdrawal threshold (MWT). It was found that macrophages and endothelial cells were functionally coupled through Epac1-p120. Adhesive linkage disorder remodeled the chronic, inflammatory, and eutrophic microenvironment at the beginning of nociceptor after operation through macrophages, endothelial cells, and endothelial paracellular pathways. It might be an early event and a key step in peripheral sensitization of CPSP. The expression of p120 in muscle tissue around the incision might become a prognostic marker for the conversion of acute postsurgical pain into CPSP. Targeted intervention of Epac1-p120 might be a clinical strategy for inhibiting the conversion of acute postsurgical pain into CPSP. Hindawi 2019-02-03 /pmc/articles/PMC6377980/ /pubmed/30863475 http://dx.doi.org/10.1155/2019/9017931 Text en Copyright © 2019 Peng Pan et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Pan, Peng Huang, Sai-Sai Shen, Shi-Ren Lu, Cui-E. Qin, Yi-Bin Zhang, Jia-Long Cao, Su Role of p120 Catenin in Epac1-Induced Chronic Postsurgical Pain in Rats |
title | Role of p120 Catenin in Epac1-Induced Chronic Postsurgical Pain in Rats |
title_full | Role of p120 Catenin in Epac1-Induced Chronic Postsurgical Pain in Rats |
title_fullStr | Role of p120 Catenin in Epac1-Induced Chronic Postsurgical Pain in Rats |
title_full_unstemmed | Role of p120 Catenin in Epac1-Induced Chronic Postsurgical Pain in Rats |
title_short | Role of p120 Catenin in Epac1-Induced Chronic Postsurgical Pain in Rats |
title_sort | role of p120 catenin in epac1-induced chronic postsurgical pain in rats |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6377980/ https://www.ncbi.nlm.nih.gov/pubmed/30863475 http://dx.doi.org/10.1155/2019/9017931 |
work_keys_str_mv | AT panpeng roleofp120catenininepac1inducedchronicpostsurgicalpaininrats AT huangsaisai roleofp120catenininepac1inducedchronicpostsurgicalpaininrats AT shenshiren roleofp120catenininepac1inducedchronicpostsurgicalpaininrats AT lucuie roleofp120catenininepac1inducedchronicpostsurgicalpaininrats AT qinyibin roleofp120catenininepac1inducedchronicpostsurgicalpaininrats AT zhangjialong roleofp120catenininepac1inducedchronicpostsurgicalpaininrats AT caosu roleofp120catenininepac1inducedchronicpostsurgicalpaininrats |