FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2017614092> ?p ?o ?g. }

• W2017614092 endingPage "208" @default.
• W2017614092 startingPage "199" @default.
• W2017614092 abstract "Abstract Previous studies have demonstrated that cGMP and cAMP reduce the endothelial permeability for fluids and macromolecules when the endothelial permeability is increased by thrombin. In this study, we have investigated the mechanism by which cGMP improves the endothelial barrier function and examined whether nitric oxide (NO) can serve as an endogenous modulator of endothelial barrier function. Thrombin increased the passage of macromolecules through human umbilical vein and human aortic endothelial cell monolayers and concomitantly increased [Ca] 2+ in vitro. Inhibition of these increases by the intracellular Ca 2+ chelator BAPTA indicated that cytoplasmic Ca 2+ elevation contributes to the thrombin-induced increase in endothelial permeability. The cGMP-dependent protein kinase activators 8-bromo-cGMP (8-Br-cGMP) and 8-(4-chlorophenylthio)cGMP (8-PCPT-cGMP) decreased the thrombin-induced passage of macromolecules. Two pathways accounted for this observation. Activation of cGMP-dependent protein kinase by 8-PCPT-cGMP decreased the accumulation of cytoplasmic Ca 2+ in aortic endothelial cells and hence reduced the thrombin-induced increase in permeability. On the other hand, in umbilical vein endothelial cells, cGMP-inhibited phosphodiesterase (PDE III) activity was mainly responsible for the cGMP-dependent reduction of endothelial permeability. The PDE III inhibitors Indolidan (LY195115) and SKF94120 decreased the thrombin-induced increase in permeability by 50% in these cells. Thrombin treatment increased cGMP formation in the majority of, but not all, cell cultures. Inhibition of NO production by N G -nitro- l- arginine methyl ester (L-NAME) enhanced the thrombin-induced increase in permeability, which was restricted to those cell cultures that displayed an increased cGMP formation after addition of thrombin. Simultaneous elevation of the endothelial cGMP concentration by atrial natriuretic factor, sodium nitroprusside, or 8-Br-cGMP prevented the additional increase in permeability induced by L-NAME. These data indicate that cGMP reduces thrombin-induced endothelial permeability by inhibition of the thrombin-induced Ca 2+ accumulation and/or by inhibition of cAMP degradation by PDE III. The relative contribution of these mechanisms differs in aortic and umbilical vein endothelial cells. NO can act in vitro as an endogenous permeability-counteracting agent by raising cGMP in endothelial cells of large vessels." @default.
• W2017614092 created "2016-06-24" @default.
• W2017614092 creator A5007102136 @default.
• W2017614092 creator A5032149465 @default.
• W2017614092 creator A5045837453 @default.
• W2017614092 creator A5083354719 @default.
• W2017614092 date "1995-02-01" @default.
• W2017614092 modified "2023-10-15" @default.
• W2017614092 title "cGMP and Nitric Oxide Modulate Thrombin-Induced Endothelial Permeability" @default.
• W2017614092 cites W1491326847 @default.
• W2017614092 cites W1518913349 @default.
• W2017614092 cites W1526187099 @default.
• W2017614092 cites W1591740791 @default.
• W2017614092 cites W1603722542 @default.
• W2017614092 cites W1795554797 @default.
• W2017614092 cites W1966322594 @default.
• W2017614092 cites W1968133040 @default.
• W2017614092 cites W1969575232 @default.
• W2017614092 cites W1971358350 @default.
• W2017614092 cites W1971631582 @default.
• W2017614092 cites W1973657843 @default.
• W2017614092 cites W1975698787 @default.
• W2017614092 cites W1977459466 @default.
• W2017614092 cites W1978094951 @default.
• W2017614092 cites W1980607109 @default.
• W2017614092 cites W1984131924 @default.
• W2017614092 cites W1990590605 @default.
• W2017614092 cites W1998766014 @default.
• W2017614092 cites W1999144431 @default.
• W2017614092 cites W2002532445 @default.
• W2017614092 cites W2007599029 @default.
• W2017614092 cites W2009751681 @default.
• W2017614092 cites W2011574071 @default.
• W2017614092 cites W2020073536 @default.
• W2017614092 cites W2021311410 @default.
• W2017614092 cites W2023021434 @default.
• W2017614092 cites W2030632713 @default.
• W2017614092 cites W2037583120 @default.
• W2017614092 cites W2053141605 @default.
• W2017614092 cites W2053841726 @default.
• W2017614092 cites W2063991043 @default.
• W2017614092 cites W2064963526 @default.
• W2017614092 cites W2071331983 @default.
• W2017614092 cites W2071605333 @default.
• W2017614092 cites W2076765669 @default.
• W2017614092 cites W2085808713 @default.
• W2017614092 cites W2092478589 @default.
• W2017614092 cites W2092929017 @default.
• W2017614092 cites W2116733912 @default.
• W2017614092 cites W2118571380 @default.
• W2017614092 cites W2131684714 @default.
• W2017614092 cites W2141260882 @default.
• W2017614092 cites W2157603347 @default.
• W2017614092 cites W2157775003 @default.
• W2017614092 cites W2305092723 @default.
• W2017614092 cites W2324004740 @default.
• W2017614092 cites W2336202838 @default.
• W2017614092 cites W2396561639 @default.
• W2017614092 cites W2398649041 @default.
• W2017614092 cites W2411456058 @default.
• W2017614092 cites W2416053388 @default.
• W2017614092 cites W2468531694 @default.
• W2017614092 cites W307883368 @default.
• W2017614092 doi "https://doi.org/10.1161/01.res.76.2.199" @default.
• W2017614092 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/7834830" @default.
• W2017614092 hasPublicationYear "1995" @default.
• W2017614092 type Work @default.
• W2017614092 sameAs 2017614092 @default.
• W2017614092 citedByCount "180" @default.
• W2017614092 countsByYear W20176140922012 @default.
• W2017614092 countsByYear W20176140922013 @default.
• W2017614092 countsByYear W20176140922014 @default.
• W2017614092 countsByYear W20176140922015 @default.
• W2017614092 countsByYear W20176140922016 @default.
• W2017614092 countsByYear W20176140922017 @default.
• W2017614092 countsByYear W20176140922018 @default.
• W2017614092 countsByYear W20176140922019 @default.
• W2017614092 countsByYear W20176140922020 @default.
• W2017614092 countsByYear W20176140922021 @default.
• W2017614092 countsByYear W20176140922022 @default.
• W2017614092 countsByYear W20176140922023 @default.
• W2017614092 crossrefType "journal-article" @default.
• W2017614092 hasAuthorship W2017614092A5007102136 @default.
• W2017614092 hasAuthorship W2017614092A5032149465 @default.
• W2017614092 hasAuthorship W2017614092A5045837453 @default.
• W2017614092 hasAuthorship W2017614092A5083354719 @default.
• W2017614092 hasConcept C120882062 @default.
• W2017614092 hasConcept C123012128 @default.
• W2017614092 hasConcept C126322002 @default.
• W2017614092 hasConcept C134018914 @default.
• W2017614092 hasConcept C184235292 @default.
• W2017614092 hasConcept C185592680 @default.
• W2017614092 hasConcept C199217515 @default.
• W2017614092 hasConcept C202751555 @default.
• W2017614092 hasConcept C2776992346 @default.
• W2017614092 hasConcept C2777292125 @default.
• W2017614092 hasConcept C2777411675 @default.
• W2017614092 hasConcept C2777834122 @default.

• next