File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Anti-inflammation therapy by activation of prostaglandin EP4 receptor in cardiovascular and other inflammatory diseases

TitleAnti-inflammation therapy by activation of prostaglandin EP4 receptor in cardiovascular and other inflammatory diseases
Authors
Keywordsaneurysms
anti-inflammation
atherosclerosis
cardiovascular diseases
chemokines
EP4
inflammation
macrophages
prostaglandin E receptor
prostaglandin E2
prostanoids
T lymphocytes
Issue Date2012
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 2012, v. 59 n. 2, p. 116-123 How to Cite?
AbstractProstaglandin E2 constitutes a major cyclooxygenase-2-derived prostanoid produced at inflammatory sites. In vitro and in vivo data support its role as a modulator of inflammation. Prostaglandin E2 exerts anti-inflammatory effects by binding to one of its receptors, the prostaglandin E receptor 4 (EP4), thereby modulating macrophage and T lymphocyte functions that participate crucially in innate and adaptive immunity and tissue remodeling and repair. The activation of EP4 suppresses the release of cytokines and chemokines from macrophages and T cells, inhibits the proliferation and the activation of T cells, and induces T-cell apoptosis. Lack of EP4 in bone marrow-derived cells accelerates local inflammation in atherosclerotic and aneurysm lesions and increases the prevalence of aneurysm formation. An EP4 agonist promotes graft survival in allograft cardiac transplantation and dampens tissue damage after myocardial ischemia. Anti-inflammatory actions of EP4 agonism may benefit other inflammatory disorders, including colitis and gastric ulcers. By contrast, EP4 acts as a proinflammatory mediator in encephalomyelitis, skin inflammation, and arthritis by promoting T helper (Th) 1 differentiation and Th17 expansion. Overall, EP4 activation produces powerful anti-inflammatory responses in many experimental diseases, rendering EP4 agonists attractive agents to attenuate syndromes associated with inflammation. Copyright © 2012 by Lippincott Williams & Wilkins.
Persistent Identifierhttp://hdl.handle.net/10722/139592
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
NIHHL-34636
HL-80472
University of Hong Kong
Funding Information:

Supported in parts by grants HL-34636 and HL-80472 (to P. L.) from NIH and by the Seed Funding Programme for Basic Research (to E. H. C. T) from The University of Hong Kong.

References

 

DC FieldValueLanguage
dc.contributor.authorTang, EHCen_HK
dc.contributor.authorLibby, Pen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorXu, Aen_HK
dc.date.accessioned2011-09-23T05:52:20Z-
dc.date.available2011-09-23T05:52:20Z-
dc.date.issued2012en_HK
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 2012, v. 59 n. 2, p. 116-123en_HK
dc.identifier.issn0160-2446en_HK
dc.identifier.urihttp://hdl.handle.net/10722/139592-
dc.description.abstractProstaglandin E2 constitutes a major cyclooxygenase-2-derived prostanoid produced at inflammatory sites. In vitro and in vivo data support its role as a modulator of inflammation. Prostaglandin E2 exerts anti-inflammatory effects by binding to one of its receptors, the prostaglandin E receptor 4 (EP4), thereby modulating macrophage and T lymphocyte functions that participate crucially in innate and adaptive immunity and tissue remodeling and repair. The activation of EP4 suppresses the release of cytokines and chemokines from macrophages and T cells, inhibits the proliferation and the activation of T cells, and induces T-cell apoptosis. Lack of EP4 in bone marrow-derived cells accelerates local inflammation in atherosclerotic and aneurysm lesions and increases the prevalence of aneurysm formation. An EP4 agonist promotes graft survival in allograft cardiac transplantation and dampens tissue damage after myocardial ischemia. Anti-inflammatory actions of EP4 agonism may benefit other inflammatory disorders, including colitis and gastric ulcers. By contrast, EP4 acts as a proinflammatory mediator in encephalomyelitis, skin inflammation, and arthritis by promoting T helper (Th) 1 differentiation and Th17 expansion. Overall, EP4 activation produces powerful anti-inflammatory responses in many experimental diseases, rendering EP4 agonists attractive agents to attenuate syndromes associated with inflammation. Copyright © 2012 by Lippincott Williams & Wilkins.en_HK
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_HK
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_HK
dc.subjectaneurysmsen_HK
dc.subjectanti-inflammationen_HK
dc.subjectatherosclerosisen_HK
dc.subjectcardiovascular diseasesen_HK
dc.subjectchemokinesen_HK
dc.subjectEP4en_HK
dc.subjectinflammationen_HK
dc.subjectmacrophagesen_HK
dc.subjectprostaglandin E receptoren_HK
dc.subjectprostaglandin E2en_HK
dc.subjectprostanoidsen_HK
dc.subjectT lymphocytesen_HK
dc.subject.meshAnti-Inflammatory Agents - pharmacology - therapeutic use-
dc.subject.meshCardiovascular Diseases - drug therapy - physiopathology-
dc.subject.meshCyclooxygenase 2 - metabolism-
dc.subject.meshInflammation - drug therapy - physiopathology-
dc.subject.meshReceptors, Prostaglandin E, EP4 Subtype - agonists - metabolism-
dc.titleAnti-inflammation therapy by activation of prostaglandin EP4 receptor in cardiovascular and other inflammatory diseasesen_HK
dc.typeArticleen_HK
dc.identifier.emailTang, EHC: evatang1@hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_HK
dc.identifier.authorityTang, EHC=rp01382en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1097/FJC.0b013e3182244a12en_HK
dc.identifier.pmid21697732-
dc.identifier.pmcidPMC3191244-
dc.identifier.scopuseid_2-s2.0-84857053651en_HK
dc.identifier.hkuros192142en_US
dc.identifier.hkuros210045-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84857053651&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume59en_HK
dc.identifier.issue2en_HK
dc.identifier.spage116en_HK
dc.identifier.epage123en_HK
dc.identifier.isiWOS:000300403000002-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTang, EHC=9536518500en_HK
dc.identifier.scopusauthoridLibby, P=7202591555en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats