Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/12629
Title: Increased aortic intimal proliferation due to MasR deletion in vitro.
Authors: Alsaadon, Hiba;Kruzliak, Peter;Smardencas, Arthur;Hayes, Alan;Bader, Michael;Angus, Peter W;Herath, Chandana B;Zulli, Anthony
Affiliation: Department of Medicine, University of Melbourne, Austin Health, Heidelberg, Vic., Australia
The Centre for Chronic Disease Prevention & Management (CCDPM), Western CHRE, Victoria University, St Albans, Vic., Australia
Department of Cardiovascular Diseases, International Clinical Research Center, St. Anne's University Hospital and Masaryk University, Brno, Czech Republic.
Max-Delbrück-Center for Molecular Medicine, Berlin-Buch, Germany.
Issue Date: 10-Feb-2015
Citation: International Journal of Experimental Pathology 2015; 96(3): 183-7
Abstract: A 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.
Internal ID Number: 25676544
URI: http://ahro.austin.org.au/austinjspui/handle/1/12629
DOI: 10.1111/iep.12118
URL: http://www.ncbi.nlm.nih.gov/pubmed/25676544
Type: Journal Article
Subjects: angiotensin (1-7) Mas receptor
atherosclerosis
endothelial function
intimal thickening
Appears in Collections:Journal articles

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