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Article: Deletion of EP4 on bone marrow-derived cells enhances inflammation and angiotensin II-induced abdominal aortic aneurysm formation

TitleDeletion of EP4 on bone marrow-derived cells enhances inflammation and angiotensin II-induced abdominal aortic aneurysm formation
Authors
Keywordsaneurysms
eicosanoids
prostaglandins
receptors
transplantation
Issue Date2011
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.lww.com/product/?1079-5642
Citation
Arteriosclerosis, Thrombosis, And Vascular Biology, 2011, v. 31 n. 2, p. 261-269 How to Cite?
AbstractObjective-: To examine whether a lack of prostaglandin E receptor 4 (EP4) on bone marrow-derived cells would increase local inflammation and enhance the formation of abdominal aortic aneurysm (AAA) in vivo. Methods and results-: Prostaglandin E2 (PGE2) through activation of EP4, can mute inflammation. Hypercholesterolemic low-density lipoprotein receptor knockout (LDLR) mice transplanted with either EP4 (EP4/LDLR) or EP4 (EP4/LDLR) bone marrow received infusions of angiotensin II to induce AAA. Deficiency of EP4 on bone marrow-derived cells increased the incidence (50% of male EP4/LDLR mice versus 88.9% of male EP4/LDLR mice developed AAA; and 22% of female EP4/LDLR mice versus 83.3% of female EP4/LDLR mice developed AAA) and severity of AAA, increased monocyte chemoattractant protein-1 (2.72-fold in males and 1.64-fold in females), and enhanced infiltration of macrophages (3.8-fold in males and 2.44-fold in females) and T cells (1.88-fold in males and 1.66-fold in females) into AAA lesions. Lack of EP4 on bone marrow-derived cells augmented elastin fragmentation, increased apoptotic markers, and decreased smooth muscle cell accumulation within AAA lesions. Conclusion-: Deficiency of EP4 on bone marrow-derived cells boosted inflammation and AAA formation induced by angiotensin II in hyperlipidemic mice. This study affirms the pathophysiologic importance of PGE2 signaling through EP4 as an endogenous anti-inflammatory pathway involved in experimental aneurysm formation. © 2011 American Heart Association, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/139593
ISSN
2015 Impact Factor: 5.969
2015 SCImago Journal Rankings: 3.356
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
National Heart, Lung, and Blood InstituteHL-34636
HL-67249
Croucher Foundation
Funding Information:

This study was supported in part by grants HL-34636 (Dr Libby) and HL-67249 (Dr Sukhova) from the National Heart, Lung, and Blood Institute; and by a fellowship from the Croucher Foundation (Dr Tang).

References

 

DC FieldValueLanguage
dc.contributor.authorTang, EHCen_HK
dc.contributor.authorShvartz, Een_HK
dc.contributor.authorShimizu, Ken_HK
dc.contributor.authorRocha, VZen_HK
dc.contributor.authorZheng, Cen_HK
dc.contributor.authorFukuda, Den_HK
dc.contributor.authorShi, GPen_HK
dc.contributor.authorSukhova, Gen_HK
dc.contributor.authorLibby, Pen_HK
dc.date.accessioned2011-09-23T05:52:20Z-
dc.date.available2011-09-23T05:52:20Z-
dc.date.issued2011en_HK
dc.identifier.citationArteriosclerosis, Thrombosis, And Vascular Biology, 2011, v. 31 n. 2, p. 261-269en_HK
dc.identifier.issn1079-5642en_HK
dc.identifier.urihttp://hdl.handle.net/10722/139593-
dc.description.abstractObjective-: To examine whether a lack of prostaglandin E receptor 4 (EP4) on bone marrow-derived cells would increase local inflammation and enhance the formation of abdominal aortic aneurysm (AAA) in vivo. Methods and results-: Prostaglandin E2 (PGE2) through activation of EP4, can mute inflammation. Hypercholesterolemic low-density lipoprotein receptor knockout (LDLR) mice transplanted with either EP4 (EP4/LDLR) or EP4 (EP4/LDLR) bone marrow received infusions of angiotensin II to induce AAA. Deficiency of EP4 on bone marrow-derived cells increased the incidence (50% of male EP4/LDLR mice versus 88.9% of male EP4/LDLR mice developed AAA; and 22% of female EP4/LDLR mice versus 83.3% of female EP4/LDLR mice developed AAA) and severity of AAA, increased monocyte chemoattractant protein-1 (2.72-fold in males and 1.64-fold in females), and enhanced infiltration of macrophages (3.8-fold in males and 2.44-fold in females) and T cells (1.88-fold in males and 1.66-fold in females) into AAA lesions. Lack of EP4 on bone marrow-derived cells augmented elastin fragmentation, increased apoptotic markers, and decreased smooth muscle cell accumulation within AAA lesions. Conclusion-: Deficiency of EP4 on bone marrow-derived cells boosted inflammation and AAA formation induced by angiotensin II in hyperlipidemic mice. This study affirms the pathophysiologic importance of PGE2 signaling through EP4 as an endogenous anti-inflammatory pathway involved in experimental aneurysm formation. © 2011 American Heart Association, Inc.en_HK
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.lww.com/product/?1079-5642en_HK
dc.relation.ispartofArteriosclerosis, Thrombosis, and Vascular Biologyen_HK
dc.subjectaneurysmsen_HK
dc.subjecteicosanoidsen_HK
dc.subjectprostaglandinsen_HK
dc.subjectreceptorsen_HK
dc.subjecttransplantationen_HK
dc.subject.meshAngiotensin II - adverse effects-
dc.subject.meshAortic Aneurysm, Abdominal - chemically induced - epidemiology - metabolism-
dc.subject.meshBone Marrow Transplantation-
dc.subject.meshInflammation - chemically induced - epidemiology - metabolism-
dc.subject.meshReceptors, Prostaglandin E, EP4 Subtype - genetics - metabolism-
dc.titleDeletion of EP4 on bone marrow-derived cells enhances inflammation and angiotensin II-induced abdominal aortic aneurysm formationen_HK
dc.typeArticleen_HK
dc.identifier.emailTang, EHC: evatang1@hku.hken_HK
dc.identifier.authorityTang, EHC=rp01382en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1161/ATVBAHA.110.216580en_HK
dc.identifier.pmid21088251-
dc.identifier.pmcidPMC3025710-
dc.identifier.scopuseid_2-s2.0-79551479091en_HK
dc.identifier.hkuros192143en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79551479091&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume31en_HK
dc.identifier.issue2en_HK
dc.identifier.spage261en_HK
dc.identifier.epage269en_HK
dc.identifier.eissn1524-4636-
dc.identifier.isiWOS:000286376800009-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTang, EHC=9536518500en_HK
dc.identifier.scopusauthoridShvartz, E=36626245200en_HK
dc.identifier.scopusauthoridShimizu, K=35392936600en_HK
dc.identifier.scopusauthoridRocha, VZ=23568679000en_HK
dc.identifier.scopusauthoridZheng, C=13606290900en_HK
dc.identifier.scopusauthoridFukuda, D=35465531500en_HK
dc.identifier.scopusauthoridShi, GP=7402432834en_HK
dc.identifier.scopusauthoridSukhova, G=35462921800en_HK
dc.identifier.scopusauthoridLibby, P=7202591555en_HK

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