Matches in SemOpenAlex for { <https://semopenalex.org/work/W2002988149> ?p ?o ?g. }
- W2002988149 endingPage "150" @default.
- W2002988149 startingPage "138" @default.
- W2002988149 abstract "Decay-accelerating factor (DAF) is a widely expressed, multifunctional cell surface protein involved in complement regulation and cell signaling. Previous studies have demonstrated that endothelial cell (EC) DAF is up-regulated by tumor necrosis factor alpha and inhibits complement binding. Because vascular endothelial growth factor (VEGF) is cytoprotective to endothelium and is expressed at sites of chronic inflammation, we hypothesized that VEGF may induce DAF expression during inflammatory angiogenesis.Human umbilical vein and dermal microvascular EC were isolated using routine procedures, and the regulation and function of DAF, as well as other complement-regulatory proteins (membrane cofactor protein and CD59), were analyzed following stimulation with VEGF.Incubation of large- or small-vessel EC with VEGF led to increased expression of DAF, with maximal expression after 48-72 hours of stimulation. This effect depended on the activation of protein kinase C (PKC) and required increased steady-state messenger RNA levels and de novo protein synthesis. Although VEGF-induced EC proliferation was inhibited by both p38 and p42/44 mitogen-activated protein kinase (MAPK) antagonists, DAF up-regulation in response to VEGF was only sensitive to inhibition of p38 MAPK. VEGF-stimulated EC showed a 60% reduction in C3 deposition following complement activation, and this resulted in a marked reduction in complement-mediated EC lysis. These protective effects were abolished by anti-DAF monoclonal antibody 1H4.This study confirms the importance of PKC for the regulation of DAF expression by EC and reveals VEGF to be a physiologic agonist for this pathway. The up-regulation of DAF expression by VEGF may represent an important mechanism for the protection of EC from complement-mediated injury during angiogenesis in inflammatory rheumatic diseases." @default.
- W2002988149 created "2016-06-24" @default.
- W2002988149 creator A5011063805 @default.
- W2002988149 creator A5011926544 @default.
- W2002988149 creator A5025544994 @default.
- W2002988149 creator A5025733594 @default.
- W2002988149 creator A5088902334 @default.
- W2002988149 date "2001-01-01" @default.
- W2002988149 modified "2023-09-29" @default.
- W2002988149 title "Induction of endothelial cell decay-accelerating factor by vascular endothelial growth factor: A mechanism for cytoprotection against complement-mediated injury during inflammatory angiogenesis" @default.
- W2002988149 cites W1500833770 @default.
- W2002988149 cites W1516140460 @default.
- W2002988149 cites W1557940991 @default.
- W2002988149 cites W1582917949 @default.
- W2002988149 cites W1589875948 @default.
- W2002988149 cites W1595344282 @default.
- W2002988149 cites W1597106254 @default.
- W2002988149 cites W1598814826 @default.
- W2002988149 cites W1620688709 @default.
- W2002988149 cites W1670891845 @default.
- W2002988149 cites W1828340002 @default.
- W2002988149 cites W1903269116 @default.
- W2002988149 cites W1966931906 @default.
- W2002988149 cites W1971281943 @default.
- W2002988149 cites W1975009096 @default.
- W2002988149 cites W1980969801 @default.
- W2002988149 cites W1982859282 @default.
- W2002988149 cites W1983395201 @default.
- W2002988149 cites W1984842433 @default.
- W2002988149 cites W1994014733 @default.
- W2002988149 cites W2001664656 @default.
- W2002988149 cites W2011403734 @default.
- W2002988149 cites W2015648136 @default.
- W2002988149 cites W2017520393 @default.
- W2002988149 cites W2024190733 @default.
- W2002988149 cites W2024237505 @default.
- W2002988149 cites W2029818075 @default.
- W2002988149 cites W2030572845 @default.
- W2002988149 cites W2031557719 @default.
- W2002988149 cites W2032731042 @default.
- W2002988149 cites W2035936653 @default.
- W2002988149 cites W2042176520 @default.
- W2002988149 cites W2045268402 @default.
- W2002988149 cites W2049746210 @default.
- W2002988149 cites W2056258832 @default.
- W2002988149 cites W2060476962 @default.
- W2002988149 cites W2067055586 @default.
- W2002988149 cites W2075553837 @default.
- W2002988149 cites W2084306312 @default.
- W2002988149 cites W2088737496 @default.
- W2002988149 cites W2091539704 @default.
- W2002988149 cites W2092523881 @default.
- W2002988149 cites W2096109479 @default.
- W2002988149 cites W2104511958 @default.
- W2002988149 cites W2109283410 @default.
- W2002988149 cites W2110678149 @default.
- W2002988149 cites W2111655511 @default.
- W2002988149 cites W2123840402 @default.
- W2002988149 cites W2140972898 @default.
- W2002988149 cites W2153048323 @default.
- W2002988149 cites W2160013986 @default.
- W2002988149 cites W2160578379 @default.
- W2002988149 cites W2161062368 @default.
- W2002988149 cites W2165061656 @default.
- W2002988149 cites W2166673618 @default.
- W2002988149 cites W2167528781 @default.
- W2002988149 cites W2178334364 @default.
- W2002988149 cites W2329991082 @default.
- W2002988149 cites W2467751620 @default.
- W2002988149 cites W4243210157 @default.
- W2002988149 cites W4294216491 @default.
- W2002988149 doi "https://doi.org/10.1002/1529-0131(200101)44:1<138::aid-anr18>3.0.co;2-g" @default.
- W2002988149 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11212152" @default.
- W2002988149 hasPublicationYear "2001" @default.
- W2002988149 type Work @default.
- W2002988149 sameAs 2002988149 @default.
- W2002988149 citedByCount "53" @default.
- W2002988149 countsByYear W20029881492012 @default.
- W2002988149 countsByYear W20029881492013 @default.
- W2002988149 countsByYear W20029881492014 @default.
- W2002988149 countsByYear W20029881492015 @default.
- W2002988149 countsByYear W20029881492016 @default.
- W2002988149 countsByYear W20029881492018 @default.
- W2002988149 countsByYear W20029881492019 @default.
- W2002988149 countsByYear W20029881492021 @default.
- W2002988149 countsByYear W20029881492022 @default.
- W2002988149 crossrefType "journal-article" @default.
- W2002988149 hasAuthorship W2002988149A5011063805 @default.
- W2002988149 hasAuthorship W2002988149A5011926544 @default.
- W2002988149 hasAuthorship W2002988149A5025544994 @default.
- W2002988149 hasAuthorship W2002988149A5025733594 @default.
- W2002988149 hasAuthorship W2002988149A5088902334 @default.
- W2002988149 hasBestOaLocation W20029881491 @default.
- W2002988149 hasConcept C111684460 @default.
- W2002988149 hasConcept C123012128 @default.
- W2002988149 hasConcept C134018914 @default.
- W2002988149 hasConcept C146285616 @default.
- W2002988149 hasConcept C15215337 @default.