Matches in SemOpenAlex for { <https://semopenalex.org/work/W2032062610> ?p ?o ?g. }
- W2032062610 endingPage "e22682" @default.
- W2032062610 startingPage "e22682" @default.
- W2032062610 abstract "Oxidative stress in the central nervous system mediates the increase in sympathetic tone that precedes the development of hypertension. We hypothesized that by transforming Angiotensin-II (AngII) into Ang-(1-7), ACE2 might reduce AngII-mediated oxidative stress in the brain and prevent autonomic dysfunction. To test this hypothesis, a relationship between ACE2 and oxidative stress was first confirmed in a mouse neuroblastoma cell line (Neuro2A cells) treated with AngII and infected with Ad-hACE2. ACE2 overexpression resulted in a reduction of reactive oxygen species (ROS) formation. In vivo, ACE2 knockout (ACE2(-/y)) mice and non-transgenic (NT) littermates were infused with AngII (10 days) and infected with Ad-hACE2 in the paraventricular nucleus (PVN). Baseline blood pressure (BP), AngII and brain ROS levels were not different between young mice (12 weeks). However, cardiac sympathetic tone, brain NADPH oxidase and SOD activities were significantly increased in ACE2(-/y). Post infusion, plasma and brain AngII levels were also significantly higher in ACE2(-/y), although BP was similarly increased in both genotypes. ROS formation in the PVN and RVLM was significantly higher in ACE2(-/y) mice following AngII infusion. Similar phenotypes, i.e. increased oxidative stress, exacerbated dysautonomia and hypertension, were also observed on baseline in mature ACE2(-/y) mice (48 weeks). ACE2 gene therapy to the PVN reduced AngII-mediated increase in NADPH oxidase activity and normalized cardiac dysautonomia in ACE2(-/y) mice. Altogether, these data indicate that ACE2 gene deletion promotes age-dependent oxidative stress, autonomic dysfunction and hypertension, while PVN-targeted ACE2 gene therapy decreases ROS formation via NADPH oxidase inhibition and improves autonomic function. Accordingly, ACE2 could represent a new target for the treatment of hypertension-associated dysautonomia and oxidative stress." @default.
- W2032062610 created "2016-06-24" @default.
- W2032062610 creator A5005660410 @default.
- W2032062610 creator A5008389654 @default.
- W2032062610 creator A5019726673 @default.
- W2032062610 creator A5050387959 @default.
- W2032062610 creator A5053197427 @default.
- W2032062610 creator A5055507597 @default.
- W2032062610 creator A5056001594 @default.
- W2032062610 creator A5081036799 @default.
- W2032062610 date "2011-07-27" @default.
- W2032062610 modified "2023-10-17" @default.
- W2032062610 title "ACE2-Mediated Reduction of Oxidative Stress in the Central Nervous System Is Associated with Improvement of Autonomic Function" @default.
- W2032062610 cites W1486361117 @default.
- W2032062610 cites W1537144565 @default.
- W2032062610 cites W1594727967 @default.
- W2032062610 cites W1964696346 @default.
- W2032062610 cites W1966409424 @default.
- W2032062610 cites W1972558089 @default.
- W2032062610 cites W1975681215 @default.
- W2032062610 cites W1977744864 @default.
- W2032062610 cites W1980058856 @default.
- W2032062610 cites W1993746543 @default.
- W2032062610 cites W1994474517 @default.
- W2032062610 cites W2000040025 @default.
- W2032062610 cites W2011200561 @default.
- W2032062610 cites W2012619772 @default.
- W2032062610 cites W2013230887 @default.
- W2032062610 cites W2014320780 @default.
- W2032062610 cites W2018211784 @default.
- W2032062610 cites W2020547131 @default.
- W2032062610 cites W2025672718 @default.
- W2032062610 cites W2027926287 @default.
- W2032062610 cites W2028468705 @default.
- W2032062610 cites W2042065946 @default.
- W2032062610 cites W2045201133 @default.
- W2032062610 cites W2053171397 @default.
- W2032062610 cites W2057150555 @default.
- W2032062610 cites W2063069042 @default.
- W2032062610 cites W2073701988 @default.
- W2032062610 cites W2075678264 @default.
- W2032062610 cites W2096540024 @default.
- W2032062610 cites W2096677035 @default.
- W2032062610 cites W2102799140 @default.
- W2032062610 cites W2103115053 @default.
- W2032062610 cites W2109740270 @default.
- W2032062610 cites W2111584700 @default.
- W2032062610 cites W2112430900 @default.
- W2032062610 cites W2118437063 @default.
- W2032062610 cites W2119494775 @default.
- W2032062610 cites W2119523842 @default.
- W2032062610 cites W2126753008 @default.
- W2032062610 cites W2134442533 @default.
- W2032062610 cites W2138138136 @default.
- W2032062610 cites W2143371349 @default.
- W2032062610 cites W2149146712 @default.
- W2032062610 cites W2150193183 @default.
- W2032062610 cites W2161399617 @default.
- W2032062610 cites W2164449616 @default.
- W2032062610 cites W2166190242 @default.
- W2032062610 cites W2169328873 @default.
- W2032062610 cites W2172010034 @default.
- W2032062610 cites W46417975 @default.
- W2032062610 doi "https://doi.org/10.1371/journal.pone.0022682" @default.
- W2032062610 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3144922" @default.
- W2032062610 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21818366" @default.
- W2032062610 hasPublicationYear "2011" @default.
- W2032062610 type Work @default.
- W2032062610 sameAs 2032062610 @default.
- W2032062610 citedByCount "107" @default.
- W2032062610 countsByYear W20320626102012 @default.
- W2032062610 countsByYear W20320626102013 @default.
- W2032062610 countsByYear W20320626102014 @default.
- W2032062610 countsByYear W20320626102015 @default.
- W2032062610 countsByYear W20320626102016 @default.
- W2032062610 countsByYear W20320626102017 @default.
- W2032062610 countsByYear W20320626102018 @default.
- W2032062610 countsByYear W20320626102019 @default.
- W2032062610 countsByYear W20320626102020 @default.
- W2032062610 countsByYear W20320626102021 @default.
- W2032062610 countsByYear W20320626102022 @default.
- W2032062610 countsByYear W20320626102023 @default.
- W2032062610 crossrefType "journal-article" @default.
- W2032062610 hasAuthorship W2032062610A5005660410 @default.
- W2032062610 hasAuthorship W2032062610A5008389654 @default.
- W2032062610 hasAuthorship W2032062610A5019726673 @default.
- W2032062610 hasAuthorship W2032062610A5050387959 @default.
- W2032062610 hasAuthorship W2032062610A5053197427 @default.
- W2032062610 hasAuthorship W2032062610A5055507597 @default.
- W2032062610 hasAuthorship W2032062610A5056001594 @default.
- W2032062610 hasAuthorship W2032062610A5081036799 @default.
- W2032062610 hasBestOaLocation W20320626101 @default.
- W2032062610 hasConcept C126322002 @default.
- W2032062610 hasConcept C134018914 @default.
- W2032062610 hasConcept C2776151105 @default.
- W2032062610 hasConcept C2777372248 @default.
- W2032062610 hasConcept C2777953023 @default.
- W2032062610 hasConcept C2779719074 @default.