Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12629
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dc.contributor.authorAlsaadon, Hiba-
dc.contributor.authorKruzliak, Peter-
dc.contributor.authorSmardencas, Arthur-
dc.contributor.authorHayes, Alan-
dc.contributor.authorBader, Michael-
dc.contributor.authorAngus, Peter W-
dc.contributor.authorHerath, Chandana B-
dc.contributor.authorZulli, Anthony-
dc.date.accessioned2015-05-16T02:21:17Z
dc.date.available2015-05-16T02:21:17Z
dc.date.issued2015-02-10-
dc.identifier.citationInternational Journal of Experimental Pathology 2015; 96(3): 183-7en_US
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/12629en
dc.description.abstractA growing body of evidence suggests that the vascular actions of Ang-(1-7) appear to involve increased production of nitric oxide (NO), an important vasodilator, through the activation of MasR, thus indicating the involvement of the MasR in preventing endothelial dysfunction. However, it is unknown whether the MasR could be involved in the progression of the next step in atherosclerosis, neo-intimal formation. To determine whether the deletion of the MasR is involved in the development of intimal thickening in an in vitro model. Mice [three background controls (C57Bl/6) and 3 MasR (-/-)] were killed and the aortas excised and cleaned of connective tissue and cut into 3 mm rings. Rings were placed in an organ culture medium for 5 weeks, embedded in paraffin, cut at 5 μm and stained with haematoxylin and eosin and Masson's trichrome. In addition, aortic reactivity was measured in organ baths. After 5 weeks of culture, the intima:media ratio increased in the aortas from MasR (-/-) mice compared to the control group by 4.5-fold (P < 0.01). However, no significant difference in nuclei area count (cell proliferation) between the MasR (-/-) mice and control group was observed (0.87 ± 0.29% vs. 0.94 ± 0.18%, respectively, P = ns). Functional studies showed only a minor vasoconstrictive and full vasodilative response. This study shows that the deletion of the MasR causes marked increase in the aortic intima:media ratio, which is not due to generalized cellular proliferation. These results provide a functional role for the MasR in atherogenesis.en_US
dc.language.isoenen
dc.subject.otherangiotensin (1-7) Mas receptoren
dc.subject.otheratherosclerosisen
dc.subject.otherendothelial functionen
dc.subject.otherintimal thickeningen
dc.titleIncreased aortic intimal proliferation due to MasR deletion in vitro.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleInternational Journal of Experimental Pathologyen_US
dc.identifier.affiliationMedicine (University of Melbourne)en_US
dc.identifier.affiliationThe Centre for Chronic Disease Prevention & Management (CCDPM), Western CHRE, Victoria University, St Albans, Victoria, Australiaen_US
dc.identifier.affiliationDepartment of Cardiovascular Diseases, International Clinical Research Center, St. Anne's University Hospital and Masaryk University, Brno, Czech Republic.en_US
dc.identifier.affiliationMax-Delbrück-Center for Molecular Medicine, Berlin-Buch, Germany.en_US
dc.identifier.doi10.1111/iep.12118en_US
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/25676544en
dc.type.contentTexten_US
dc.type.austinJournal Articleen
local.name.researcherAngus, Peter W
item.languageiso639-1en-
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.cerifentitytypePublications-
crisitem.author.deptVictorian Liver Transplant Unit-
crisitem.author.deptGastroenterology and Hepatology-
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