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Transgenic mice overexpressing Semicarbazide-sensitive amine oxidase (SSAO) have an elevated pulse pressure
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Neuroscience.
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Manuscript (Other academic)
URN: urn:nbn:se:uu:diva-92399OAI: oai:DiVA.org:uu-92399DiVA: diva2:165455
Available from: 2004-11-18 Created: 2004-11-18 Last updated: 2010-01-13Bibliographically approved
In thesis
1. Semicarbazide-sensitive Amine Oxidase (SSAO) – Regulation and Involvement in Blood Vessel Damage with Special Regard to Diabetes: A Study on Mice Overexpressing Human SSAO
Open this publication in new window or tab >>Semicarbazide-sensitive Amine Oxidase (SSAO) – Regulation and Involvement in Blood Vessel Damage with Special Regard to Diabetes: A Study on Mice Overexpressing Human SSAO
2004 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Semicarbazide-sensitive amine oxidase (SSAO, EC belongs to a family of copper-containing amine oxidases. SSAO exists as a membrane bound protein in endothelial-, smooth muscle-, and adipose cells as well as soluble in plasma. SSAO catalyses oxidative deamination of primary monoamines, which results in the production of corresponding aldehydes, hydrogen peroxide and ammonia. These compounds are very reactive and potentially cytotoxic, and are able to induce vascular damage if produced in high levels. Patients with diabetes mellitus, and with diabetic complications in particular, have a higher SSAO activity in plasma compared to healthy controls. It has therefore been speculated that high SSAO activity is involved in the development of vascular complications associated with diabetes. The aim of this thesis is to investigate the importance of SSAO in the development of disorders of a vascular origin. We have studied the transcriptional regulation of the SSAO gene, by inducing diabetes in NMRI and in transgenic mice, overexpressing the human form of SSAO in smooth muscle cells. We found that the increase in SSAO activity in diabetes is accompanied by reduced mRNA levels of the endogenous mouse gene, suggesting a negative feedback on the transcription of the SSAO gene. In addition, the transgenic mice exhibited an abnormal phenotype in the elastic tissue of aorta and renal artery. These mice have a lower mean artery pressure and an elevated pulse pressure. These results indicate that high SSAO activity in smooth muscle cells is associated with a change in the morphology of large arteries. This is likely contributing to the development of vascular complications in diabetes.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2004. 54 p.
Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 0282-7476 ; 1391
Pharmacology, amine oxidases, VAP-1, vascular complications, diabetes, blood pressure, Farmakologi
National Category
Pharmacology and Toxicology
urn:nbn:se:uu:diva-4673 (URN)91-554-6098-4 (ISBN)
Public defence
2004-12-10, Room B41, Building A4, BMC, Husargatan 3, Uppsala, 09:15
Available from: 2004-11-18 Created: 2004-11-18Bibliographically approved

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