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Consequences of altered eicosanoid patterns for nociceptive processing in mPGES-1-deficient mice
Cyclooxygenase-2 (COX-2)-dependent prostaglandin (PG) E(2) synthesis in the spinal cord plays a major role in the development of inflammatory hyperalgesia and allodynia. Microsomal PGE(2) synthase-1 (mPGES-1) isomerizes COX-2-derived PGH(2) to PGE(2). Here, we evaluated the effect of mPGES-1-deficie...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Blackwell Publishing Ltd
2008
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3822549/ https://www.ncbi.nlm.nih.gov/pubmed/18419601 http://dx.doi.org/10.1111/j.1582-4934.2007.00110.x |
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author | Brenneis, Christian Coste, Ovidiu Schmidt, Ronald Angioni, Carlo Popp, Laura Nusing, Rolf M Becker, Wiebke Scholich, Klaus Geisslinger, Gerd |
author_facet | Brenneis, Christian Coste, Ovidiu Schmidt, Ronald Angioni, Carlo Popp, Laura Nusing, Rolf M Becker, Wiebke Scholich, Klaus Geisslinger, Gerd |
author_sort | Brenneis, Christian |
collection | PubMed |
description | Cyclooxygenase-2 (COX-2)-dependent prostaglandin (PG) E(2) synthesis in the spinal cord plays a major role in the development of inflammatory hyperalgesia and allodynia. Microsomal PGE(2) synthase-1 (mPGES-1) isomerizes COX-2-derived PGH(2) to PGE(2). Here, we evaluated the effect of mPGES-1-deficiency on the noci-ceptive behavior in various models of nociception that depend on PGE(2) synthesis. Surprisingly, in the COX-2-dependent zymosan-evoked hyperalgesia model, the nociceptive behavior was not reduced in mPGES-1-deficient mice despite a marked decrease of the spinal PGE(2) synthesis. Similarly, the nociceptive behavior was unaltered in mPGES-1-deficient mice in the formalin test. Importantly, spinal cords and primary spinal cord cells derived from mPGES-1-deficient mice showed a redirection of the PGE(2) synthesis to PGD(2), PGF(2α) and 6-keto-PGF(1α) (stable metabolite of PGI(2)). Since the latter prostaglandins serve also as mediators of noci-ception they may compensate the loss of PGE(2) synthesis in mPGES-1-deficient mice. |
format | Online Article Text |
id | pubmed-3822549 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | Blackwell Publishing Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-38225492015-04-27 Consequences of altered eicosanoid patterns for nociceptive processing in mPGES-1-deficient mice Brenneis, Christian Coste, Ovidiu Schmidt, Ronald Angioni, Carlo Popp, Laura Nusing, Rolf M Becker, Wiebke Scholich, Klaus Geisslinger, Gerd J Cell Mol Med Images in Cellular / Molecular Medicine Cyclooxygenase-2 (COX-2)-dependent prostaglandin (PG) E(2) synthesis in the spinal cord plays a major role in the development of inflammatory hyperalgesia and allodynia. Microsomal PGE(2) synthase-1 (mPGES-1) isomerizes COX-2-derived PGH(2) to PGE(2). Here, we evaluated the effect of mPGES-1-deficiency on the noci-ceptive behavior in various models of nociception that depend on PGE(2) synthesis. Surprisingly, in the COX-2-dependent zymosan-evoked hyperalgesia model, the nociceptive behavior was not reduced in mPGES-1-deficient mice despite a marked decrease of the spinal PGE(2) synthesis. Similarly, the nociceptive behavior was unaltered in mPGES-1-deficient mice in the formalin test. Importantly, spinal cords and primary spinal cord cells derived from mPGES-1-deficient mice showed a redirection of the PGE(2) synthesis to PGD(2), PGF(2α) and 6-keto-PGF(1α) (stable metabolite of PGI(2)). Since the latter prostaglandins serve also as mediators of noci-ception they may compensate the loss of PGE(2) synthesis in mPGES-1-deficient mice. Blackwell Publishing Ltd 2008-04 2007-08-31 /pmc/articles/PMC3822549/ /pubmed/18419601 http://dx.doi.org/10.1111/j.1582-4934.2007.00110.x Text en ©2008 The Authors Journal compilation © 2008 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd |
spellingShingle | Images in Cellular / Molecular Medicine Brenneis, Christian Coste, Ovidiu Schmidt, Ronald Angioni, Carlo Popp, Laura Nusing, Rolf M Becker, Wiebke Scholich, Klaus Geisslinger, Gerd Consequences of altered eicosanoid patterns for nociceptive processing in mPGES-1-deficient mice |
title | Consequences of altered eicosanoid patterns for nociceptive processing in mPGES-1-deficient mice |
title_full | Consequences of altered eicosanoid patterns for nociceptive processing in mPGES-1-deficient mice |
title_fullStr | Consequences of altered eicosanoid patterns for nociceptive processing in mPGES-1-deficient mice |
title_full_unstemmed | Consequences of altered eicosanoid patterns for nociceptive processing in mPGES-1-deficient mice |
title_short | Consequences of altered eicosanoid patterns for nociceptive processing in mPGES-1-deficient mice |
title_sort | consequences of altered eicosanoid patterns for nociceptive processing in mpges-1-deficient mice |
topic | Images in Cellular / Molecular Medicine |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3822549/ https://www.ncbi.nlm.nih.gov/pubmed/18419601 http://dx.doi.org/10.1111/j.1582-4934.2007.00110.x |
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