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Soluble epoxide hydrolase and epoxyeicosatrienoic acids modulate two distinct analgesic pathways.

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Title: Soluble epoxide hydrolase and epoxyeicosatrienoic acids modulate two distinct analgesic pathways.
Authors: Inceoglu, Bora1, Jinks, Steven L.2, UIu, Arzu1, Hegedus, Christine M.1, Georgi, Katrin1, Schmelzer, Kara R.1, Wagner, Karen1, Jones, Paul D.1, Morisseau, Christophe1, Hammock, Bruce D.1 bdhammock@ucdavis.edu
Source: Proceedings of the National Academy of Sciences of the United States of America. 12/2/2008, Vol. 105 Issue 48, p18901-18906. 6p. 1 Diagram, 2 Graphs.
Subjects: Inflammation, Arachidonic acid, Cyclooxygenases, Prostaglandins, Cytochromes, Messenger RNA
Abstract: During inflammation, a large amount of arachidonic acid (AA) is released into the cellular milieu and cyclooxygenase enzymes convert this AA to prostaglandins that in turn sensitize pain pathways. However, AA is also converted to natural epoxyeicosatrienoic acids (EEls) by cytochrome P450 enzymes. EET levels are typically regulated by soluble epoxide hydrolase (5EH), the major enzyme degrading EET5. Here we demonstrate that EET5 or inhibition of sEH lead to antihyperalgesia by at least 2 spinal mechanisms, first by repressing the induction of the COX2 gene and second by rapidly up-regulating an acute neurosteroid-producing gene, StARD1, which requires the synchronized presence of elevated cAMP and EEl levels. The analgesic activities of neurosteroids are well known; however, here we describe a clear course toward augmenting the levels of these molecules. Redirecting the flow of pronociceptive intracellular cAMP toward up-regulation of StARD1 mRNA by concomitantly elevating EET5 is a novel path to accomplish pain relief in both inflammatory and neuropathic pain states. [ABSTRACT FROM AUTHOR]
Copyright of Proceedings of the National Academy of Sciences of the United States of America is the property of National Academy of Sciences and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Engineering Source
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DbLabel: Engineering Source
An: 35760713
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PubType: Academic Journal
PubTypeId: academicJournal
PreciseRelevancyScore: 0
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  Data: Soluble epoxide hydrolase and epoxyeicosatrienoic acids modulate two distinct analgesic pathways.
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  Data: <searchLink fieldCode="JN" term="%22Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America%22">Proceedings of the National Academy of Sciences of the United States of America</searchLink>. 12/2/2008, Vol. 105 Issue 48, p18901-18906. 6p. 1 Diagram, 2 Graphs.
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  Data: <searchLink fieldCode="DE" term="%22Inflammation%22">Inflammation</searchLink><br /><searchLink fieldCode="DE" term="%22Arachidonic+acid%22">Arachidonic acid</searchLink><br /><searchLink fieldCode="DE" term="%22Cyclooxygenases%22">Cyclooxygenases</searchLink><br /><searchLink fieldCode="DE" term="%22Prostaglandins%22">Prostaglandins</searchLink><br /><searchLink fieldCode="DE" term="%22Cytochromes%22">Cytochromes</searchLink><br /><searchLink fieldCode="DE" term="%22Messenger+RNA%22">Messenger RNA</searchLink>
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  Data: During inflammation, a large amount of arachidonic acid (AA) is released into the cellular milieu and cyclooxygenase enzymes convert this AA to prostaglandins that in turn sensitize pain pathways. However, AA is also converted to natural epoxyeicosatrienoic acids (EEls) by cytochrome P450 enzymes. EET levels are typically regulated by soluble epoxide hydrolase (5EH), the major enzyme degrading EET5. Here we demonstrate that EET5 or inhibition of sEH lead to antihyperalgesia by at least 2 spinal mechanisms, first by repressing the induction of the COX2 gene and second by rapidly up-regulating an acute neurosteroid-producing gene, StARD1, which requires the synchronized presence of elevated cAMP and EEl levels. The analgesic activities of neurosteroids are well known; however, here we describe a clear course toward augmenting the levels of these molecules. Redirecting the flow of pronociceptive intracellular cAMP toward up-regulation of StARD1 mRNA by concomitantly elevating EET5 is a novel path to accomplish pain relief in both inflammatory and neuropathic pain states. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Proceedings of the National Academy of Sciences of the United States of America is the property of National Academy of Sciences and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1073/pnas.0809765105
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        Text: English
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        Type: general
      – SubjectFull: Arachidonic acid
        Type: general
      – SubjectFull: Cyclooxygenases
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      – SubjectFull: Cytochromes
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      – SubjectFull: Messenger RNA
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      – TitleFull: Soluble epoxide hydrolase and epoxyeicosatrienoic acids modulate two distinct analgesic pathways.
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              M: 12
              Text: 12/2/2008
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