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EphrinB/EphB signaling contributes to spinal nociceptive processing via calpain-1 and caspase-3
Previous studies have indicated that an important subfamily of receptor tyrosine kinases, ephrins and their receptors, are important in pain signaling, particularly in spinal nociceptive processing. In the present study, the role of the ephrin/Eph signaling pathway was confirmed, and it was shown th...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6059679/ https://www.ncbi.nlm.nih.gov/pubmed/29749521 http://dx.doi.org/10.3892/mmr.2018.8996 |
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author | Yang, Mei Chen, Wei Zhang, Yu Yang, Rui Wang, Yiru Yuan, Hongbin |
author_facet | Yang, Mei Chen, Wei Zhang, Yu Yang, Rui Wang, Yiru Yuan, Hongbin |
author_sort | Yang, Mei |
collection | PubMed |
description | Previous studies have indicated that an important subfamily of receptor tyrosine kinases, ephrins and their receptors, are important in pain signaling, particularly in spinal nociceptive processing. In the present study, the role of the ephrin/Eph signaling pathway was confirmed, and it was shown that this signaling was also involved in spinal nociceptive processing through the actions of calpain-1 and caspase-3. First, the ephrinB ligands, ephrinB1-Fc or ephrinB2-Fc, were introduced into experimental mice via intrathecal injection, and it was found that this injection induced marked time- and dose-dependent mechanical allodynia and thermal hyperalgesia, accompanied by increased levels of calpain-1 and caspase-3 in the spinal cord. MDL28170, an inhibitor of calpain-1, reversed the behavioral effects and ameliorated the increases in calpain-1 and caspase-3. Second, it was found that the administration of EphB1 between L5 and L6 in mice inhibited the mechanical allodynia and thermal hyperalgesia induced by chronic constrictive injury. In addition, to demonstrate the cell phenotypes responsible for the increased levels of calpain-1 and caspase-3 in the spinal cord following injection with ephrinB2-Fc, double immunofluorescent labeling was performed, which indicated that calpain-1 and caspase-3 were localized in neurons, but not in astrocytes or microglial cells. In conclusion, the present study suggested that ephrinB/EphB signaling contributes to spinal nociceptive processing via the actions of calpain-1 and caspase-3. |
format | Online Article Text |
id | pubmed-6059679 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-60596792018-07-26 EphrinB/EphB signaling contributes to spinal nociceptive processing via calpain-1 and caspase-3 Yang, Mei Chen, Wei Zhang, Yu Yang, Rui Wang, Yiru Yuan, Hongbin Mol Med Rep Articles Previous studies have indicated that an important subfamily of receptor tyrosine kinases, ephrins and their receptors, are important in pain signaling, particularly in spinal nociceptive processing. In the present study, the role of the ephrin/Eph signaling pathway was confirmed, and it was shown that this signaling was also involved in spinal nociceptive processing through the actions of calpain-1 and caspase-3. First, the ephrinB ligands, ephrinB1-Fc or ephrinB2-Fc, were introduced into experimental mice via intrathecal injection, and it was found that this injection induced marked time- and dose-dependent mechanical allodynia and thermal hyperalgesia, accompanied by increased levels of calpain-1 and caspase-3 in the spinal cord. MDL28170, an inhibitor of calpain-1, reversed the behavioral effects and ameliorated the increases in calpain-1 and caspase-3. Second, it was found that the administration of EphB1 between L5 and L6 in mice inhibited the mechanical allodynia and thermal hyperalgesia induced by chronic constrictive injury. In addition, to demonstrate the cell phenotypes responsible for the increased levels of calpain-1 and caspase-3 in the spinal cord following injection with ephrinB2-Fc, double immunofluorescent labeling was performed, which indicated that calpain-1 and caspase-3 were localized in neurons, but not in astrocytes or microglial cells. In conclusion, the present study suggested that ephrinB/EphB signaling contributes to spinal nociceptive processing via the actions of calpain-1 and caspase-3. D.A. Spandidos 2018-07 2018-05-09 /pmc/articles/PMC6059679/ /pubmed/29749521 http://dx.doi.org/10.3892/mmr.2018.8996 Text en Copyright: © Yang 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 Yang, Mei Chen, Wei Zhang, Yu Yang, Rui Wang, Yiru Yuan, Hongbin EphrinB/EphB signaling contributes to spinal nociceptive processing via calpain-1 and caspase-3 |
title | EphrinB/EphB signaling contributes to spinal nociceptive processing via calpain-1 and caspase-3 |
title_full | EphrinB/EphB signaling contributes to spinal nociceptive processing via calpain-1 and caspase-3 |
title_fullStr | EphrinB/EphB signaling contributes to spinal nociceptive processing via calpain-1 and caspase-3 |
title_full_unstemmed | EphrinB/EphB signaling contributes to spinal nociceptive processing via calpain-1 and caspase-3 |
title_short | EphrinB/EphB signaling contributes to spinal nociceptive processing via calpain-1 and caspase-3 |
title_sort | ephrinb/ephb signaling contributes to spinal nociceptive processing via calpain-1 and caspase-3 |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6059679/ https://www.ncbi.nlm.nih.gov/pubmed/29749521 http://dx.doi.org/10.3892/mmr.2018.8996 |
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