FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1653219913> ?p ?o ?g. }

• W1653219913 endingPage "723" @default.
• W1653219913 startingPage "711" @default.
• W1653219913 abstract "Aims: Vascular oxidative stress generated by endothelial NO synthase (eNOS) was observed in experimental and clinical cardiovascular disease, but its relative importance for vascular pathologies is unclear. We investigated the impact of eNOS-dependent vascular oxidative stress on endothelial function and on neointimal hyperplasia. Results: A dimer-destabilized mutant of bovine eNOS where cysteine 101 was replaced by alanine was cloned and introduced into an eNOS-deficient mouse strain (eNOS-KO) in an endothelial-specific manner. Destabilization of mutant eNOS in cells and eNOS-KO was confirmed by the reduced dimer/monomer ratio. Purified mutant eNOS and transfected cells generated less citrulline and NO, respectively, while superoxide generation was enhanced. In eNOS-KO, introduction of mutant eNOS caused a 2.3–3.7-fold increase in superoxide and peroxynitrite formation in the aorta and myocardium. This was completely blunted by an NOS inhibitor. Nevertheless, expression of mutant eNOS in eNOS-KO completely restored maximal aortic endothelium-dependent relaxation to acetylcholine. Neointimal hyperplasia induced by carotid binding was much larger in eNOS-KO than in mutant eNOS-KO and C57BL/6, while the latter strains showed comparable hyperplasia. Likewise, vascular remodeling was blunted in eNOS-KO only. Innovation: Our results provide the first in vivo evidence that eNOS-dependent oxidative stress is unlikely to be an initial cause of impaired endothelium-dependent vasodilation and/or a pathologic factor promoting intimal hyperplasia. These findings highlight the importance of other sources of vascular oxidative stress in cardiovascular disease. Conclusion: eNOS-dependent oxidative stress is unlikely to induce functional vascular damage as long as concomitant generation of NO is preserved. This underlines the importance of current and new therapeutic strategies in improving endothelial NO generation. Antioxid. Redox Signal. 23, 711–723." @default.
• W1653219913 created "2016-06-24" @default.
• W1653219913 creator A5003712662 @default.
• W1653219913 creator A5014119597 @default.
• W1653219913 creator A5016571719 @default.
• W1653219913 creator A5040392090 @default.
• W1653219913 creator A5067430418 @default.
• W1653219913 creator A5069780164 @default.
• W1653219913 creator A5082087707 @default.
• W1653219913 creator A5087422548 @default.
• W1653219913 creator A5091664271 @default.
• W1653219913 date "2015-09-20" @default.
• W1653219913 modified "2023-09-26" @default.
• W1653219913 title "Impact of eNOS-Dependent Oxidative Stress on Endothelial Function and Neointima Formation" @default.
• W1653219913 cites W113714250 @default.
• W1653219913 cites W130347995 @default.
• W1653219913 cites W1479676079 @default.
• W1653219913 cites W1602409208 @default.
• W1653219913 cites W1946153048 @default.
• W1653219913 cites W1963782920 @default.
• W1653219913 cites W1964526269 @default.
• W1653219913 cites W1972789975 @default.
• W1653219913 cites W1974332277 @default.
• W1653219913 cites W1974729135 @default.
• W1653219913 cites W1982033190 @default.
• W1653219913 cites W1982203562 @default.
• W1653219913 cites W1982235892 @default.
• W1653219913 cites W1987686985 @default.
• W1653219913 cites W1992277607 @default.
• W1653219913 cites W1995521498 @default.
• W1653219913 cites W1997023449 @default.
• W1653219913 cites W2004175200 @default.
• W1653219913 cites W2011089437 @default.
• W1653219913 cites W2011200561 @default.
• W1653219913 cites W2011863986 @default.
• W1653219913 cites W2018643804 @default.
• W1653219913 cites W2021294790 @default.
• W1653219913 cites W2026425756 @default.
• W1653219913 cites W2033896075 @default.
• W1653219913 cites W2036086294 @default.
• W1653219913 cites W2037586146 @default.
• W1653219913 cites W2042800607 @default.
• W1653219913 cites W2044259132 @default.
• W1653219913 cites W2045148129 @default.
• W1653219913 cites W2045982598 @default.
• W1653219913 cites W2050548878 @default.
• W1653219913 cites W2051329265 @default.
• W1653219913 cites W2053734625 @default.
• W1653219913 cites W2063024150 @default.
• W1653219913 cites W2071812057 @default.
• W1653219913 cites W2075308691 @default.
• W1653219913 cites W2076345713 @default.
• W1653219913 cites W2083037047 @default.
• W1653219913 cites W2089730495 @default.
• W1653219913 cites W2091499945 @default.
• W1653219913 cites W2093455882 @default.
• W1653219913 cites W2095368090 @default.
• W1653219913 cites W2095968162 @default.
• W1653219913 cites W2103636227 @default.
• W1653219913 cites W2104790006 @default.
• W1653219913 cites W2109544293 @default.
• W1653219913 cites W2111340450 @default.
• W1653219913 cites W2115135910 @default.
• W1653219913 cites W2120261914 @default.
• W1653219913 cites W2128368203 @default.
• W1653219913 cites W2143995396 @default.
• W1653219913 cites W2149968000 @default.
• W1653219913 cites W2158779536 @default.
• W1653219913 cites W2161952636 @default.
• W1653219913 cites W2166155183 @default.
• W1653219913 cites W2167513859 @default.
• W1653219913 cites W2169182236 @default.
• W1653219913 cites W2214291492 @default.
• W1653219913 cites W2263537973 @default.
• W1653219913 cites W2324841714 @default.
• W1653219913 cites W4245679605 @default.
• W1653219913 doi "https://doi.org/10.1089/ars.2014.6059" @default.
• W1653219913 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4580305" @default.
• W1653219913 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25764009" @default.
• W1653219913 hasPublicationYear "2015" @default.
• W1653219913 type Work @default.
• W1653219913 sameAs 1653219913 @default.
• W1653219913 citedByCount "27" @default.
• W1653219913 countsByYear W16532199132015 @default.
• W1653219913 countsByYear W16532199132016 @default.
• W1653219913 countsByYear W16532199132017 @default.
• W1653219913 countsByYear W16532199132018 @default.
• W1653219913 countsByYear W16532199132019 @default.
• W1653219913 countsByYear W16532199132020 @default.
• W1653219913 countsByYear W16532199132021 @default.
• W1653219913 countsByYear W16532199132022 @default.
• W1653219913 countsByYear W16532199132023 @default.
• W1653219913 crossrefType "journal-article" @default.
• W1653219913 hasAuthorship W1653219913A5003712662 @default.
• W1653219913 hasAuthorship W1653219913A5014119597 @default.
• W1653219913 hasAuthorship W1653219913A5016571719 @default.
• W1653219913 hasAuthorship W1653219913A5040392090 @default.
• W1653219913 hasAuthorship W1653219913A5067430418 @default.

• next