Sökning: onr:"swepub:oai:DiVA.org:uu-4673" >
Semicarbazide-sensi...
-
Göktürk, Camilla,1967-Uppsala universitet,Institutionen för neurovetenskap
(författare)
Semicarbazide-sensitive Amine Oxidase (SSAO) – Regulation and Involvement in Blood Vessel Damage with Special Regard to Diabetes : A Study on Mice Overexpressing Human SSAO
Förlag, utgivningsår, omfång ...
-
Uppsala :Acta Universitatis Upsaliensis,2004
-
54 s.
-
electronicrdacarrier
Nummerbeteckningar
-
LIBRIS-ID:oai:DiVA.org:uu-4673
-
ISBN:9155460984
-
https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4673URI
Kompletterande språkuppgifter
-
Språk:engelska
-
Sammanfattning på:engelska
Ingår i deldatabas
Klassifikation
-
Ämneskategori:vet swepub-contenttype
-
Ämneskategori:dok swepub-publicationtype
Serie
-
Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine,0282-7476 ;1391
Anmärkningar
-
Semicarbazide-sensitive amine oxidase (SSAO, EC 1.4.3.6) 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.
Ämnesord och genrebeteckningar
Biuppslag (personer, institutioner, konferenser, titlar ...)
-
Oreland, Lars
(preses)
-
Forsberg-Nilsson, Karin
(preses)
-
Larhammar, Dan
(preses)
-
Yu, Peter,ProfessorNeuro Psychiatry Research Unit, Saskatchewan, Canada
(opponent)
-
Uppsala universitetInstitutionen för neurovetenskap
(creator_code:org_t)
Internetlänk
Hitta via bibliotek
Till lärosätets databas