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Status: Bibliographieeintrag

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Verfasst von:Buday, Anna [VerfasserIn]   i
 Őrsy, Petra [VerfasserIn]   i
 Godó, Mária [VerfasserIn]   i
 Mózes, Miklós [VerfasserIn]   i
 Kökény, Gábor [VerfasserIn]   i
 Lacza, Zsombor [VerfasserIn]   i
 Koller, Ákos [VerfasserIn]   i
 Ungvári, Zoltán [VerfasserIn]   i
 Groß-Weissmann, Marie-Luise [VerfasserIn]   i
 Benyó, Zoltán [VerfasserIn]   i
 Hamar, Péter [VerfasserIn]   i
Titel:Elevated systemic TGF-β impairs aortic vasomotor function through activation of NADPH oxidase-driven superoxide production and leads to hypertension, myocardial remodeling, and increased plaque formation in apoE−/− mice
Verf.angabe:Anna Buday, Petra Őrsy, Mária Godó, Miklós Mózes, Gábor Kökény, Zsombor Lacza, Ákos Koller, Zoltán Ungvári, Marie-Luise Gross, Zoltán Benyó, and Péter Hamar
E-Jahr:2010
Jahr:May 28, 2010
Umfang:10 S.
Fussnoten:Im Titel ist "−/−" hochgestellt ; Gesehen am 15.03.2023
Titel Quelle:Enthalten in: American journal of physiology / Heart and circulatory physiology
Ort Quelle:Bethesda, Md. : American Physiological Society, 1977
Jahr Quelle:2010
Band/Heft Quelle:299(2010), 2, Seite H386-H395
ISSN Quelle:1522-1539
Abstract:The role of circulating, systemic TGF-β levels in endothelial function is not clear. TGF-β1 may cause endothelial dysfunction in apolipoprotein E-deficient (apoE−/−) mice via stimulation of reactive oxygen species (ROS) production by the NADPH oxidase (NOX) system and aggravate aortic and heart remodeling and hypertension. Thoracic aorta (TA) were isolated from 4-mo-old control (C57Bl/6), apoE−/−, TGF-β1-overexpressing (TGFβ1), and crossbred apoE−/− × TGFβ1 mice. Endothelium-dependent relaxation was measured before and after incubation with apocynin (NOX inhibitor) or superoxide dismutase (SOD; ROS scavenger). Superoxide production within the vessel wall was determined by dihydroethidine staining under confocal microscope. In 8-mo-old mice, aortic and myocardial morphometric changes, plaque formation by en face fat staining, and blood pressure were determined. Serum TGF-β1 levels (ELISA) were elevated in TGFβ1 mice without downregulation of TGF-β-I receptor (immunohistochemistry). In the aortic wall, superoxide production was enhanced and NO-dependent relaxation diminished in apoE−/− × TGFβ1 mice but improved significantly after apocynin or SOD. Myocardial capillary density was reduced, fibrocyte density increased, aortic wall was thicker, combined lesion area was greater, and blood pressure was higher in the apoE−/− × TGFβ vs. C57Bl/6 mice. Our results demonstrate that elevated circulating TGF-β1 causes endothelial dysfunction through NOX activation-induced oxidative stress, accelerating atherosclerosis and hypertension in apoE−/− mice. These findings may provide a mechanism explaining accelerated atherosclerosis in patients with elevated plasma TGFβ1.
DOI:doi:10.1152/ajpheart.01042.2009
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1152/ajpheart.01042.2009
 Volltext: https://journals.physiology.org/doi/full/10.1152/ajpheart.01042.2009
 DOI: https://doi.org/10.1152/ajpheart.01042.2009
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:aorta
 apolipoprotein E-deficient mice
 nicotinamide adenine dinucleotide phosphate
 oxidative stress
 transforming growth factor-β
K10plus-PPN:1839271817
Verknüpfungen:→ Zeitschrift

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