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Conference Paper: Over-expression of endothelin-1 in astrocytes, but not endothelial cells, ameliorates inflammatory pain response after formalin injection

TitleOver-expression of endothelin-1 in astrocytes, but not endothelial cells, ameliorates inflammatory pain response after formalin injection
Authors
KeywordsEndothelin-1
Astrocytes
Endothelial cells
Inflammatory pain
Issue Date2012
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie
Citation
The 12th International Conference on Endothelin (ET-12), Cambridge, UK, 11-14 September 2011. In Life Sciences, 2012, v. 91 n. 13–14, p. 618-622 How to Cite?
AbstractAims Endothelin-1 (ET-1) has been suggested to be involved in different types of pain due to its neuromodulatory nature. However, its role in inflammatory pain processing, specifically the origin-specific effect, has not yet been clearly defined. Therefore, the aim of this study is to determine the role of cell-type specific ET-1 induction in the modulation of inflammatory pain processing. Main methods The current study assesses the effects of ET-1 over-expression specifically targeted to astrocytes (GET-1) or endothelial cells (TET-1) on the expression of pain-like behaviors induced by a model of inflammatory pain, consisting of a formalin injection into the hind paw. Key findings The baseline sensitivity thresholds of GET-1 and TET-1 mice to the response elicited by tactile and radiant heat stimulation were similar to those observed in age-matched non-transgenic (NTg) controls. Relative to the NTg controls, GET-1 mice displayed a marked decrease in pain-like behavioral responses during the second phase of formalin-induced pain (i.e., 15–20 min after injection), whereas the responses elicited in TET-1 mice were unaltered. The levels of mRNA encoding adrenomedullin, calcitonin gene-related peptide and calcitonin-like receptor were elevated in the spinal cord of saline-injected GET-1 mice compared to those of NTg mice. Significance The current results support a suppressor role for astrocyte-derived ET-1 in inflammatory pain and suggest that the study of GET-1 mice might provide mechanistic insights for improving the treatment of inflammatory pain.
Persistent Identifierhttp://hdl.handle.net/10722/249600
ISSN
2019 Impact Factor: 3.647
2015 SCImago Journal Rankings: 1.056
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHung, KL-
dc.contributor.authorChen, SMY-
dc.contributor.authorTai, LW-
dc.contributor.authorChen, AYS-
dc.contributor.authorChung, SK-
dc.contributor.authorCheung, CW-
dc.date.accessioned2017-11-21T03:04:27Z-
dc.date.available2017-11-21T03:04:27Z-
dc.date.issued2012-
dc.identifier.citationThe 12th International Conference on Endothelin (ET-12), Cambridge, UK, 11-14 September 2011. In Life Sciences, 2012, v. 91 n. 13–14, p. 618-622-
dc.identifier.issn0024-3205-
dc.identifier.urihttp://hdl.handle.net/10722/249600-
dc.description.abstractAims Endothelin-1 (ET-1) has been suggested to be involved in different types of pain due to its neuromodulatory nature. However, its role in inflammatory pain processing, specifically the origin-specific effect, has not yet been clearly defined. Therefore, the aim of this study is to determine the role of cell-type specific ET-1 induction in the modulation of inflammatory pain processing. Main methods The current study assesses the effects of ET-1 over-expression specifically targeted to astrocytes (GET-1) or endothelial cells (TET-1) on the expression of pain-like behaviors induced by a model of inflammatory pain, consisting of a formalin injection into the hind paw. Key findings The baseline sensitivity thresholds of GET-1 and TET-1 mice to the response elicited by tactile and radiant heat stimulation were similar to those observed in age-matched non-transgenic (NTg) controls. Relative to the NTg controls, GET-1 mice displayed a marked decrease in pain-like behavioral responses during the second phase of formalin-induced pain (i.e., 15–20 min after injection), whereas the responses elicited in TET-1 mice were unaltered. The levels of mRNA encoding adrenomedullin, calcitonin gene-related peptide and calcitonin-like receptor were elevated in the spinal cord of saline-injected GET-1 mice compared to those of NTg mice. Significance The current results support a suppressor role for astrocyte-derived ET-1 in inflammatory pain and suggest that the study of GET-1 mice might provide mechanistic insights for improving the treatment of inflammatory pain.-
dc.languageeng-
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie-
dc.relation.ispartofLife Sciences-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectEndothelin-1-
dc.subjectAstrocytes-
dc.subjectEndothelial cells-
dc.subjectInflammatory pain-
dc.titleOver-expression of endothelin-1 in astrocytes, but not endothelial cells, ameliorates inflammatory pain response after formalin injection-
dc.typeConference_Paper-
dc.identifier.emailChung, SK: skchung@hkucc.hku.hk-
dc.identifier.emailCheung, CW: cheucw@hku.hk-
dc.identifier.authorityChung, SK=rp00381-
dc.identifier.authorityCheung, CW=rp00244-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1016/j.lfs.2012.06.038-
dc.identifier.pmid22820168-
dc.identifier.hkuros282981-
dc.identifier.hkuros228165-
dc.identifier.hkuros204274-
dc.identifier.volume91-
dc.identifier.issue13–14-
dc.identifier.spage618-
dc.identifier.epage622-
dc.identifier.isiWOS:000310115300025-
dc.publisher.placeUnited States-

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