FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2793166129> ?p ?o ?g. }

• W2793166129 endingPage "116" @default.
• W2793166129 startingPage "105" @default.
• W2793166129 abstract "Interferon (IFN)-α and IFN-β approved for treatment of chronic hepatitis C viral infection and multiple sclerosis respectively have been linked to thrombotic microangiopathy (TMA) affecting renal function. Since the molecular mechanisms underlying this severe complication remain largely unclear, we aimed to investigate whether IFN affects directly in vitro endothelial cell functions associated with angiogenesis and blood haemostasis, as well as endothelial cell-derived vasodilators of nitric oxide (NO) and prostacyclin.Proliferation and survival of human umbilical vein endothelial cells (HUVECs) were measured by BrdU incorporation and alamarBlue assays. Angiogenesis was evaluated in co-cultures of HUVECs and human dermal fibroblasts. Fibrinolysis molecules were measured with ELISA. NO and prostacyclin were measured using a fluorescent NO-specific probe and a competitive enzyme immunoassay, respectively.HUVEC proliferation was dose-dependently inhibited by IFN-β1a and IFN-β1b, but not by IFN-α2a and IFN-α2b. Consistently, IFN-β1a and IFN-β1b also reduced survival of HUVECs, but this again was not observed with IFN-α. However, both IFN subtypes inhibited VEGF-induced development of capillary-like structures, but the effect of IFN-α was less potent than IFN-β. In addition, both IFN subtypes upregulated interferon inducible protein 10 production from treated co-cultures while suppressing angiogenesis. Furthermore, intracellular NO generation was reduced by IFN-α2a and IFN-β1a, whereas prostacyclin release from HUVECs was not affected by IFN. Importantly, both IFN-β1a- and IFN-β1b-treated HUVECs showed a marked reduction in urokinase-type plasminogen activator release and a much greater secretion of plasminogen activator inhibitor-1 than tissue-type plasminogen activator compared with untreated cells, suggesting decreased fibrinolytic activity. IFN-α, however was less effective in modulating the fibrinolysis system.We demonstrate the detrimental effects of IFN on endothelial cell functions mediated with angiogenesis and fibrinolysis, which could potentially cause the loss of physiological endothelium thromboresistance and facilitate the development of vascular complications in a clinical setting. Mechanistically, our findings have implications for understanding how IFN therapy can foster the development of TMA." @default.
• W2793166129 created "2018-03-29" @default.
• W2793166129 creator A5026557059 @default.
• W2793166129 creator A5028833382 @default.
• W2793166129 creator A5033739869 @default.
• W2793166129 creator A5054975682 @default.
• W2793166129 creator A5066913564 @default.
• W2793166129 creator A5071763668 @default.
• W2793166129 date "2018-03-01" @default.
• W2793166129 modified "2023-09-25" @default.
• W2793166129 title "Endothelial cell functions impaired by interferon in vitro: Insights into the molecular mechanism of thrombotic microangiopathy associated with interferon therapy" @default.
• W2793166129 cites W1509956588 @default.
• W2793166129 cites W1560599335 @default.
• W2793166129 cites W1600721209 @default.
• W2793166129 cites W1606252645 @default.
• W2793166129 cites W1643585163 @default.
• W2793166129 cites W1843606951 @default.
• W2793166129 cites W1968858361 @default.
• W2793166129 cites W1969052771 @default.
• W2793166129 cites W1970623463 @default.
• W2793166129 cites W1973720975 @default.
• W2793166129 cites W1982003857 @default.
• W2793166129 cites W1995737060 @default.
• W2793166129 cites W1995827857 @default.
• W2793166129 cites W1998956477 @default.
• W2793166129 cites W2004181624 @default.
• W2793166129 cites W2006950015 @default.
• W2793166129 cites W2008456809 @default.
• W2793166129 cites W2013637340 @default.
• W2793166129 cites W2019472095 @default.
• W2793166129 cites W2028031291 @default.
• W2793166129 cites W2038139581 @default.
• W2793166129 cites W2043304383 @default.
• W2793166129 cites W2059504760 @default.
• W2793166129 cites W2067181405 @default.
• W2793166129 cites W2070041397 @default.
• W2793166129 cites W2071196780 @default.
• W2793166129 cites W2071981343 @default.
• W2793166129 cites W2073107052 @default.
• W2793166129 cites W2075527727 @default.
• W2793166129 cites W2081474310 @default.
• W2793166129 cites W2094919000 @default.
• W2793166129 cites W2098769806 @default.
• W2793166129 cites W2102047778 @default.
• W2793166129 cites W2103465511 @default.
• W2793166129 cites W2106273198 @default.
• W2793166129 cites W2111218879 @default.
• W2793166129 cites W2119129191 @default.
• W2793166129 cites W2121698544 @default.
• W2793166129 cites W2122995291 @default.
• W2793166129 cites W2151463001 @default.
• W2793166129 cites W2154900633 @default.
• W2793166129 cites W2158791216 @default.
• W2793166129 cites W2164797072 @default.
• W2793166129 cites W2169932958 @default.
• W2793166129 cites W2201917454 @default.
• W2793166129 cites W2328043056 @default.
• W2793166129 cites W2478788944 @default.
• W2793166129 cites W2508007259 @default.
• W2793166129 cites W2521316545 @default.
• W2793166129 cites W2527258465 @default.
• W2793166129 cites W2556359407 @default.
• W2793166129 cites W2557184605 @default.
• W2793166129 cites W2571785753 @default.
• W2793166129 cites W2587798070 @default.
• W2793166129 cites W2742614612 @default.
• W2793166129 cites W86035162 @default.
• W2793166129 doi "https://doi.org/10.1016/j.thromres.2018.01.039" @default.
• W2793166129 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29407621" @default.
• W2793166129 hasPublicationYear "2018" @default.
• W2793166129 type Work @default.
• W2793166129 sameAs 2793166129 @default.
• W2793166129 citedByCount "33" @default.
• W2793166129 countsByYear W27931661292018 @default.
• W2793166129 countsByYear W27931661292019 @default.
• W2793166129 countsByYear W27931661292020 @default.
• W2793166129 countsByYear W27931661292021 @default.
• W2793166129 countsByYear W27931661292022 @default.
• W2793166129 countsByYear W27931661292023 @default.
• W2793166129 crossrefType "journal-article" @default.
• W2793166129 hasAuthorship W2793166129A5026557059 @default.
• W2793166129 hasAuthorship W2793166129A5028833382 @default.
• W2793166129 hasAuthorship W2793166129A5033739869 @default.
• W2793166129 hasAuthorship W2793166129A5054975682 @default.
• W2793166129 hasAuthorship W2793166129A5066913564 @default.
• W2793166129 hasAuthorship W2793166129A5071763668 @default.
• W2793166129 hasBestOaLocation W27931661291 @default.
• W2793166129 hasConcept C123012128 @default.
• W2793166129 hasConcept C134018914 @default.
• W2793166129 hasConcept C202751555 @default.
• W2793166129 hasConcept C203014093 @default.
• W2793166129 hasConcept C2776178377 @default.
• W2793166129 hasConcept C2777411675 @default.
• W2793166129 hasConcept C2777834122 @default.
• W2793166129 hasConcept C2779679481 @default.
• W2793166129 hasConcept C2780394083 @default.
• W2793166129 hasConcept C2781128415 @default.
• W2793166129 hasConcept C502942594 @default.

• next