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Conference Paper: Role of exchange protein directly activated by cAMP 1 & 2 (Epac1 & Epac2) in inflammatory pain

TitleRole of exchange protein directly activated by cAMP 1 & 2 (Epac1 & Epac2) in inflammatory pain
Authors
Issue Date2016
PublisherThe University of Hong Kong.
Citation
The 2016 Neuroscience Symposium and Annual Scientific Conference of the Hong Kong Society of Neurosciences, The University of Hong Kong, Hong Kong, 18 May 2016. In Programme Book, 2016, p. 52, abstract no. P44 How to Cite?
Abstract3’-5’-cyclic adenosine monophosphate (cAMP) is a key mediator of nociceptor signaling. There is evidence that Epac mediates cAMP signaling under inflammatory conditions, however, the significance of the two isoforms of Epac, Epac1 and Epac2, in inflammatory pain is unclear. In the present study, Epac1 (Epac1-/-) and Epac2 (Epac2-/-)-deficient mice were used to study the role of Epac in formalin-induced inflammatory pain. Here, we report that Epac1-/- and Epac2-/- mice display significantly lower nociceptor behavior compared to the wild-type (Epac1+/+; 2+/+) mice under formalin-induced inflammatory conditions. Cyclooxygenase-2 (Cox-2) protein was significantly overexpressed in the ipsilateral sciatic nerve of the Epac1+/+; 2+/+, but not Epac2-/- mice. Cox-2 is rapidly induced due to inflammation and is known to sensitize nociceptors leading to increased pain sensitivity. Collectively, these data suggest that Epac2 deficiency alleviates pain by preventing Cox2 induction. Furthermore, phosphorylated ERK protein expression was found to be significantly reduced in the ipsilateral DRG of Epac2-/- mice, suggesting that the Epac2 deficiency leads to suppression of formalin-induced ERK phosphorylation in the DRG. Our findings indicate the involvement of both Epac1 and Epac2 in inflammation-induced hyperalgesia in animals, and suggest that Epac could potentially be a novel therapeutic target for the treatment of pain.
DescriptionConference Theme: Nature and Nurture in Brain Functions
Persistent Identifierhttp://hdl.handle.net/10722/231521

 

DC FieldValueLanguage
dc.contributor.authorVirwani, PD-
dc.contributor.authorZhou, L-
dc.contributor.authorWang, Y-
dc.contributor.authorChung, SK-
dc.date.accessioned2016-09-20T05:23:42Z-
dc.date.available2016-09-20T05:23:42Z-
dc.date.issued2016-
dc.identifier.citationThe 2016 Neuroscience Symposium and Annual Scientific Conference of the Hong Kong Society of Neurosciences, The University of Hong Kong, Hong Kong, 18 May 2016. In Programme Book, 2016, p. 52, abstract no. P44-
dc.identifier.urihttp://hdl.handle.net/10722/231521-
dc.descriptionConference Theme: Nature and Nurture in Brain Functions-
dc.description.abstract3’-5’-cyclic adenosine monophosphate (cAMP) is a key mediator of nociceptor signaling. There is evidence that Epac mediates cAMP signaling under inflammatory conditions, however, the significance of the two isoforms of Epac, Epac1 and Epac2, in inflammatory pain is unclear. In the present study, Epac1 (Epac1-/-) and Epac2 (Epac2-/-)-deficient mice were used to study the role of Epac in formalin-induced inflammatory pain. Here, we report that Epac1-/- and Epac2-/- mice display significantly lower nociceptor behavior compared to the wild-type (Epac1+/+; 2+/+) mice under formalin-induced inflammatory conditions. Cyclooxygenase-2 (Cox-2) protein was significantly overexpressed in the ipsilateral sciatic nerve of the Epac1+/+; 2+/+, but not Epac2-/- mice. Cox-2 is rapidly induced due to inflammation and is known to sensitize nociceptors leading to increased pain sensitivity. Collectively, these data suggest that Epac2 deficiency alleviates pain by preventing Cox2 induction. Furthermore, phosphorylated ERK protein expression was found to be significantly reduced in the ipsilateral DRG of Epac2-/- mice, suggesting that the Epac2 deficiency leads to suppression of formalin-induced ERK phosphorylation in the DRG. Our findings indicate the involvement of both Epac1 and Epac2 in inflammation-induced hyperalgesia in animals, and suggest that Epac could potentially be a novel therapeutic target for the treatment of pain.-
dc.languageeng-
dc.publisherThe University of Hong Kong.-
dc.relation.ispartofNeuroscience Symposium & Annual Scientific Conference of the Hong Kong Society of Neurosciences-
dc.titleRole of exchange protein directly activated by cAMP 1 & 2 (Epac1 & Epac2) in inflammatory pain-
dc.typeConference_Paper-
dc.identifier.emailZhou, L: lenazhou@hku.hk-
dc.identifier.emailWang, Y: yuwanghk@hku.hk-
dc.identifier.emailChung, SK: skchung@hkucc.hku.hk-
dc.identifier.authorityWang, Y=rp00239-
dc.identifier.authorityChung, SK=rp00381-
dc.identifier.hkuros266395-
dc.identifier.spage52, abstract no. P44-
dc.identifier.epage52, abstract no. P44-
dc.publisher.placeHong Kong-

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