About: Genetic Deletion of ACE2 Induces Vascular Dysfunction in C57BL/6 Mice: Role of Nitric Oxide Imbalance and Oxidative Stress

Facets (new session)
Description
Metadata
Settings
- owl:sameAs
- Inference Rule:

About: Genetic Deletion of ACE2 Induces Vascular Dysfunction in C57BL/6 Mice: Role of Nitric Oxide Imbalance and Oxidative Stress Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Genetic Deletion of ACE2 Induces Vascular Dysfunction in C57BL/6 Mice: Role of Nitric Oxide Imbalance and Oxidative Stress
Creator	Bader, Michael Nunes-Souza, Valéria Alenina, Natalia Gollasch, Maik Penninger, Josef Qadri, Fatimunnisa Rabelo, Luiza Santos, Robson Szijártó, István Todiras, Mihail
source	PMC
abstract	Accumulating evidence indicates that angiotensin-converting enzyme 2 (ACE2) plays a critical role in cardiovascular homeostasis, and its altered expression is associated with major cardiac and vascular disorders. The aim of this study was to evaluate the regulation of vascular function and assess the vascular redox balance in ACE2-deficient (ACE2(-/y)) animals. Experiments were performed in 20–22 week-old C57BL/6 and ACE2(-/y) male mice. Evaluation of endothelium-dependent and -independent relaxation revealed an impairment of in vitro and in vivo vascular function in ACE2(-/y) mice. Drastic reduction in eNOS expression at both protein and mRNA levels, and a decrease in (•)NO concentrations were observed in aortas of ACE2(-/y) mice in comparison to controls. Consistently, these mice presented a lower plasma and urine nitrite concentration, confirming reduced (•)NO availability in ACE2-deficient animals. Lipid peroxidation was significantly increased and superoxide dismutase activity was decreased in aorta homogenates of ACE2(-/y) mice, indicating impaired antioxidant capacity. Taken together, our data indicate, that ACE2 regulates vascular function by modulating nitric oxide release and oxidative stress. In conclusion, we elucidate mechanisms by which ACE2 is involved in the maintenance of vascular homeostasis. Furthermore, these findings provide insights into the role of the renin-angiotensin system in both vascular and systemic redox balance.
has issue date	2016-04-12(xsd:dateTime)
bibo:doi	10.1371/journal.pone.0150255
bibo:pmid	27070147
has license	cc-by
sha1sum (hex)	c5745c2eaaf8e94e31a179ce4e8775a3cd0e6745
schema:url	https://doi.org/10.1371/journal.pone.0150255
resource representing a document's title	Genetic Deletion of ACE2 Induces Vascular Dysfunction in C57BL/6 Mice: Role of Nitric Oxide Imbalance and Oxidative Stress
has PubMed Central identifier	PMC4829150
has PubMed identifier	27070147
schema:publication	PLoS One
resource representing a document's body	covid:c5745c2eaaf8e94e31a179ce4e8775a3cd0e6745#body_text
is schema:about of	named entity 'vascular' named entity 'oxidative stress' named entity 'mice' named entity 'performed' named entity 'mice' named entity 'revealed' covid:arg/c5745c2eaaf8e94e31a179ce4e8775a3cd0e6745 named entity 'function' named entity 'redox' named entity 'protein' named entity 'endothelium' named entity 'xylazine' named entity 'dose-response curves' named entity 'eNOS' named entity 'proinflammatory' named entity 'AT1' named entity 'NOx' named entity 'reduction-oxidation' named entity 'endothelial' named entity 'ACE2' named entity 'argon laser' named entity 'vascular dilatation' named entity 'ACE2' named entity 'enzyme' named entity 'Mannheim' named entity 'ANOVA' named entity 'Männedorf' named entity 'aortas' named entity 'urinary concentration' named entity 'genetic deletion' named entity 'eNOS' named entity 'ACh' named entity 'AKT' named entity '2.0' named entity 'RAS' named entity 'primers' named entity 'oxidative stress' named entity 'homogenates' named entity 'ACE2' named entity 'endothelial function' named entity 'endothelium' named entity 'endothelial function' named entity 'heart rate' named entity 'nitric oxide' named entity 'Small Vessel' named entity 'endothelial dysfunction' named entity 'ACE2' named entity 'humidified' named entity 'blood pressure regulation' named entity 'nitric oxide' named entity 'ACE2' named entity 'SOD' named entity 'ACE2' named entity 'bioavailability' named entity 'C57BL/6' named entity 'intracellular' named entity 'malondialdehyde' named entity 'phosphorylated' named entity 'SNP' named entity 'cardiovascular' named entity 'nitric oxide' named entity 'AKT pathway' named entity 'hypertensive' named entity 'μmol' named entity 'ACE2' named entity 'polyethylene glycol' named entity 'elevated blood pressure' named entity 'aorta' named entity 'reduced levels' named entity 'NOx' named entity 'exogenous' named entity 'P<0.05'

Faceted Search & Find service v1.13.91 as of Mar 24 2020

Alternative Linked Data Documents: Sponger | ODE Content Formats:

RDF

ODATA

Microdata

About

OpenLink Virtuoso version 07.20.3229 as of Jul 10 2020, on Linux (x86_64-pc-linux-gnu), Single-Server Edition (94 GB total memory)
Data on this page belongs to its respective rights holders.
Virtuoso Faceted Browser Copyright © 2009-2025 OpenLink Software