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Article: Differential secretion of prostaglandin E2, thromboxane A 2and interleukin-6 in intact and ruptured abdominal aortic aneurysms

TitleDifferential secretion of prostaglandin E2, thromboxane A 2and interleukin-6 in intact and ruptured abdominal aortic aneurysms
Authors
Issue Date2007
PublisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/IJMM/ijmm.htm
Citation
International Journal Of Molecular Medicine, 2007, v. 20 n. 3, p. 391-395 How to Cite?
AbstractRuptured abdominal aortic aneurysm (AAA) contributes largely to aneurysm-related morbidity and mortality. An inflammatory gene, COX-2, was found to be widely expressed in AAA. However, the involvement of COX-2 metabolites and other inflammatory mediators in the disease and particularly in AAA rupture still needs elucidation. The purpose of the present study was to evaluate the secretion of inflammatory mediators and the expression of macrophages in aneurysms and determine their significance in ruptured AAA. Aortic tissue was harvested at time of aortic reconstructive surgery for the group of intact AAA (n=20) and ruptured AAA (n=10) or at time of organ harvest for normal aortic tissue (n=4). Aortic explant cultures were immediately established and the culture medium was collected after 72 h. Specific enzyme-linked immunoassorbent assays were used to quantify COX-2 metabolites and inflammatory cytokines. Inflammatory macrophage cells were also quantified in the corresponding aortic walls immunohistochemically. Differences in the secretory levels of inflammatory metabolites and the macrophage quantity in all groups were assessed. All three explant culture groups secreted detectable levels of studied COX-2 metabolites, including PGE2, PGF2α, PGI2 and TxB 2 and inflammatory cytokines, including interleukin (IL)-1β, IL-6, IL-8 and IL-10. The secretory levels of PGE2, TXB2 and IL-6 were highest in the ruptured AAA explant cultures and statistically higher than those in intact AAA cultures (p>0.05). The secretion of those inflammatory mediators and the local expression of macrophages in ruptured aneurysm probably reflects the active inflammatory processes in the aortic lesions. A means of modifying the inflammatory process in the wall of AAAs might play an important role in preventing aneurysm rupture.
Persistent Identifierhttp://hdl.handle.net/10722/169748
ISSN
2015 Impact Factor: 2.348
2015 SCImago Journal Rankings: 0.868
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheuk, BLYen_US
dc.contributor.authorCheng, SWKen_US
dc.date.accessioned2012-10-25T04:54:49Z-
dc.date.available2012-10-25T04:54:49Z-
dc.date.issued2007en_US
dc.identifier.citationInternational Journal Of Molecular Medicine, 2007, v. 20 n. 3, p. 391-395en_US
dc.identifier.issn1107-3756en_US
dc.identifier.urihttp://hdl.handle.net/10722/169748-
dc.description.abstractRuptured abdominal aortic aneurysm (AAA) contributes largely to aneurysm-related morbidity and mortality. An inflammatory gene, COX-2, was found to be widely expressed in AAA. However, the involvement of COX-2 metabolites and other inflammatory mediators in the disease and particularly in AAA rupture still needs elucidation. The purpose of the present study was to evaluate the secretion of inflammatory mediators and the expression of macrophages in aneurysms and determine their significance in ruptured AAA. Aortic tissue was harvested at time of aortic reconstructive surgery for the group of intact AAA (n=20) and ruptured AAA (n=10) or at time of organ harvest for normal aortic tissue (n=4). Aortic explant cultures were immediately established and the culture medium was collected after 72 h. Specific enzyme-linked immunoassorbent assays were used to quantify COX-2 metabolites and inflammatory cytokines. Inflammatory macrophage cells were also quantified in the corresponding aortic walls immunohistochemically. Differences in the secretory levels of inflammatory metabolites and the macrophage quantity in all groups were assessed. All three explant culture groups secreted detectable levels of studied COX-2 metabolites, including PGE2, PGF2α, PGI2 and TxB 2 and inflammatory cytokines, including interleukin (IL)-1β, IL-6, IL-8 and IL-10. The secretory levels of PGE2, TXB2 and IL-6 were highest in the ruptured AAA explant cultures and statistically higher than those in intact AAA cultures (p>0.05). The secretion of those inflammatory mediators and the local expression of macrophages in ruptured aneurysm probably reflects the active inflammatory processes in the aortic lesions. A means of modifying the inflammatory process in the wall of AAAs might play an important role in preventing aneurysm rupture.en_US
dc.languageengen_US
dc.publisherDemetrios A Spandidos Ed & Pub. The Journal's web site is located at http://147.52.72.117/IJMM/ijmm.htmen_US
dc.relation.ispartofInternational Journal of Molecular Medicineen_US
dc.subject.meshAgeden_US
dc.subject.meshAortic Aneurysm, Abdominal - Etiology - Pathology - Physiopathologyen_US
dc.subject.meshAortic Rupture - Etiology - Pathology - Physiopathologyen_US
dc.subject.meshCyclooxygenase 2 - Metabolismen_US
dc.subject.meshDinoprostone - Secretionen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshInflammation Mediators - Metabolismen_US
dc.subject.meshInterleukin-6 - Secretionen_US
dc.subject.meshMacrophages - Pathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshThromboxane A2 - Secretionen_US
dc.subject.meshTissue Culture Techniquesen_US
dc.titleDifferential secretion of prostaglandin E2, thromboxane A 2and interleukin-6 in intact and ruptured abdominal aortic aneurysmsen_US
dc.typeArticleen_US
dc.identifier.emailCheuk, BLY: bernice@hku.hken_US
dc.identifier.emailCheng, SWK: wkcheng@hkucc.hku.hken_US
dc.identifier.authorityCheuk, BLY=rp01671en_US
dc.identifier.authorityCheng, SWK=rp00374en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid17671746-
dc.identifier.scopuseid_2-s2.0-35148887226en_US
dc.identifier.hkuros138354-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-35148887226&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume20en_US
dc.identifier.issue3en_US
dc.identifier.spage391en_US
dc.identifier.epage395en_US
dc.identifier.isiWOS:000248699900017-
dc.publisher.placeGreeceen_US
dc.identifier.scopusauthoridCheuk, BLY=7801343617en_US
dc.identifier.scopusauthoridCheng, SWK=7404684779en_US

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