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Conference Paper: Prostaglandin E2-EP4 signaling reduces inflammation in mouse adipose tissue

TitleProstaglandin E2-EP4 signaling reduces inflammation in mouse adipose tissue
Authors
KeywordsMedical sciences
Cardiovascular diseases
Issue Date2012
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVR
Citation
EDHF 2012 - 10th Anniversary Meeting, Vaux-de-Cernay, France, 27-30 June 2012. In Journal of Vascular Research, 2012, v. 49 suppl. 2, abstract no. 46 How to Cite?
Abstract
Inflammation of adipose tissue plays a causative role in inducing metabolic syndrome associated with obesity. Thus examining ways to control or inhibit adipose tissue inflammation is of clinical interest. In the present study, we were interested to see if endogenous prostaglandin E2 (PGE2) modulates inflammation via activation of EP4 receptors in mouse adipose tissue. PGE2 (5-500nM) attenuated lipopolysaccharide (LPS)-induced mRNA and protein expression of chemokines in mouse adipose tissue, including interferon-γ-inducible protein 10 (IP10) and macrophage-inflammatory protein (MIP)-1α. Such response was reversed with L161,982 (100nM, a selective EP4 antagonist), mimicked with two structurally different selective EP4 agonists [CAY10580 (10μM) and CAY10598 (10μM)], and was absence in adipose tissue derived from EP4-deficient mice. These findings consolidated the requirement of EP4 in the response. PGE2 significantly reduced LPS-induced chemokines in mature adipocytes, rather than in stromal vascular cells. Antiinflammatory effect of PGE2 in adipose tissue was mimicked with 8-bromo-cyclic adenosine monophosphoate (cAMP) but was insensitive to H98 (a protein kinase A inhibitor). The use of adipose tissue from high-fat fed mice confirmed that EP4-dependent anti-inflammatory response is sustained during diet-induced obesity. Furthermore, adipose tissue and systemic inflammation is enhanced in high-fat fed EP4 deficient mice as compared to wild-type littermates, providing in vivo evidences that PGE2-EP4 signaling modulates inflammation. Our work illustrated that PGE2 via activation of EP4 is a potential endogenous anti-inflammatory mediator in mouse adipose tissue and targeting EP4 could be a strategy to mitigate adipose tissue inflammation.
DescriptionThis journal suppl. contain abstracts of EDHF 2012 - 10th Anniversary Meeting
Persistent Identifierhttp://hdl.handle.net/10722/165459
ISSN
2013 Impact Factor: 2.443

 

DC FieldValueLanguage
dc.contributor.authorTang, EHCen_US
dc.contributor.authorWong, CKen_US
dc.contributor.authorXu, Aen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-09-20T08:18:22Z-
dc.date.available2012-09-20T08:18:22Z-
dc.date.issued2012en_US
dc.identifier.citationEDHF 2012 - 10th Anniversary Meeting, Vaux-de-Cernay, France, 27-30 June 2012. In Journal of Vascular Research, 2012, v. 49 suppl. 2, abstract no. 46en_US
dc.identifier.issn1018-1172-
dc.identifier.urihttp://hdl.handle.net/10722/165459-
dc.descriptionThis journal suppl. contain abstracts of EDHF 2012 - 10th Anniversary Meeting-
dc.description.abstractInflammation of adipose tissue plays a causative role in inducing metabolic syndrome associated with obesity. Thus examining ways to control or inhibit adipose tissue inflammation is of clinical interest. In the present study, we were interested to see if endogenous prostaglandin E2 (PGE2) modulates inflammation via activation of EP4 receptors in mouse adipose tissue. PGE2 (5-500nM) attenuated lipopolysaccharide (LPS)-induced mRNA and protein expression of chemokines in mouse adipose tissue, including interferon-γ-inducible protein 10 (IP10) and macrophage-inflammatory protein (MIP)-1α. Such response was reversed with L161,982 (100nM, a selective EP4 antagonist), mimicked with two structurally different selective EP4 agonists [CAY10580 (10μM) and CAY10598 (10μM)], and was absence in adipose tissue derived from EP4-deficient mice. These findings consolidated the requirement of EP4 in the response. PGE2 significantly reduced LPS-induced chemokines in mature adipocytes, rather than in stromal vascular cells. Antiinflammatory effect of PGE2 in adipose tissue was mimicked with 8-bromo-cyclic adenosine monophosphoate (cAMP) but was insensitive to H98 (a protein kinase A inhibitor). The use of adipose tissue from high-fat fed mice confirmed that EP4-dependent anti-inflammatory response is sustained during diet-induced obesity. Furthermore, adipose tissue and systemic inflammation is enhanced in high-fat fed EP4 deficient mice as compared to wild-type littermates, providing in vivo evidences that PGE2-EP4 signaling modulates inflammation. Our work illustrated that PGE2 via activation of EP4 is a potential endogenous anti-inflammatory mediator in mouse adipose tissue and targeting EP4 could be a strategy to mitigate adipose tissue inflammation.-
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVR-
dc.relation.ispartofJournal of Vascular Researchen_US
dc.rightsJournal of Vascular Research. Copyright © S Karger AG.-
dc.subjectMedical sciences-
dc.subjectCardiovascular diseases-
dc.titleProstaglandin E2-EP4 signaling reduces inflammation in mouse adipose tissueen_US
dc.typeConference_Paperen_US
dc.identifier.emailTang, EHC: evatang1@hku.hken_US
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_US
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_US
dc.identifier.authorityTang, EHC=rp01382en_US
dc.identifier.authorityXu, A=rp00485en_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.identifier.hkuros211041en_US
dc.identifier.hkuros201393-
dc.identifier.volume49-
dc.identifier.issuesuppl. 2-
dc.publisher.placeSwitzerland-

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