FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2113158483> ?p ?o ?g. }

• W2113158483 endingPage "245" @default.
• W2113158483 startingPage "236" @default.
• W2113158483 abstract "Rheumatoid arthritis (RA) is a chronic autoimmune disease with high morbidity and mortality. Within the inflammatory milieu, resident fibroblast-like synoviocytes (FLS) in the synovial tissue undergo hyperplasia, which leads to joint destruction. Epidemiologic studies and our previous research suggest that activation of the aryl hydrocarbon receptor (AHR) pathway plays an instrumental role in the inflammatory and destructive RA phenotype. In addition, our recent studies implicate the AHR in the regulation of the expression of several growth factors in established tumor cell lines. Thus, under inflammatory conditions, we hypothesized that the AHR is involved in the constitutive and inducible expression of several growth factors, FLS proliferation and migration, along with protease-dependent invasion in FLS from patients with RA (RA-FLS). Treatment with the AHR antagonist GNF351 inhibits cytokine-induced expression of vascular endothelial growth factor-A (VEGF-A), epiregulin, amphiregulin, and basic fibroblast growth factor mRNA through an AHR-dependent mechanism in both RA-FLS and FLS. Secretion of VEGF-A and epiregulin from RA-FLS was also inhibited upon GNF351 treatment. RA-FLS cell migration, along with cytokine-induced RA-FLS cell proliferation, was significantly attenuated by GNF351 exposure. Treatment of RA-FLS with GNF351 mitigated cytokine-mediated expression of matrix metalloproteinase-2 and -9 mRNA and diminished the RA-FLS invasive phenotype. These findings indicate that inhibition of AHR activity may be a viable therapeutic target in amelioration of disease progression in RA by attenuating growth factor release; FLS proliferation, migration, and invasion; and inflammatory activity." @default.
• W2113158483 created "2016-06-24" @default.
• W2113158483 creator A5034523396 @default.
• W2113158483 creator A5039686326 @default.
• W2113158483 creator A5039936196 @default.
• W2113158483 creator A5045765971 @default.
• W2113158483 creator A5048058203 @default.
• W2113158483 creator A5054584608 @default.
• W2113158483 creator A5064767923 @default.
• W2113158483 creator A5080630073 @default.
• W2113158483 creator A5081069263 @default.
• W2113158483 creator A5086342318 @default.
• W2113158483 date "2013-12-05" @default.
• W2113158483 modified "2023-09-25" @default.
• W2113158483 title "Aryl Hydrocarbon Receptor Antagonism Attenuates Growth Factor Expression, Proliferation, and Migration in Fibroblast-Like Synoviocytes from Patients with Rheumatoid Arthritis" @default.
• W2113158483 cites W1508837702 @default.
• W2113158483 cites W1903872164 @default.
• W2113158483 cites W1929633615 @default.
• W2113158483 cites W1968072906 @default.
• W2113158483 cites W1971944674 @default.
• W2113158483 cites W1986090515 @default.
• W2113158483 cites W1990336673 @default.
• W2113158483 cites W1994174953 @default.
• W2113158483 cites W1995755401 @default.
• W2113158483 cites W2000468514 @default.
• W2113158483 cites W2001965435 @default.
• W2113158483 cites W2002667904 @default.
• W2113158483 cites W2005832407 @default.
• W2113158483 cites W2006713993 @default.
• W2113158483 cites W2007867222 @default.
• W2113158483 cites W2010042266 @default.
• W2113158483 cites W2015472059 @default.
• W2113158483 cites W2016561878 @default.
• W2113158483 cites W2024497106 @default.
• W2113158483 cites W2040568539 @default.
• W2113158483 cites W2041311874 @default.
• W2113158483 cites W2043091055 @default.
• W2113158483 cites W2055073146 @default.
• W2113158483 cites W2055928479 @default.
• W2113158483 cites W2057325749 @default.
• W2113158483 cites W2057545937 @default.
• W2113158483 cites W2082562728 @default.
• W2113158483 cites W2084672116 @default.
• W2113158483 cites W2092728238 @default.
• W2113158483 cites W2094654739 @default.
• W2113158483 cites W2097615954 @default.
• W2113158483 cites W2098423712 @default.
• W2113158483 cites W2103819978 @default.
• W2113158483 cites W2106974808 @default.
• W2113158483 cites W2109440685 @default.
• W2113158483 cites W2117475605 @default.
• W2113158483 cites W2122643576 @default.
• W2113158483 cites W2134257736 @default.
• W2113158483 cites W2144678247 @default.
• W2113158483 cites W2145304191 @default.
• W2113158483 cites W2151701775 @default.
• W2113158483 cites W2152273843 @default.
• W2113158483 cites W2156531916 @default.
• W2113158483 cites W2158412843 @default.
• W2113158483 doi "https://doi.org/10.1124/jpet.113.209726" @default.
• W2113158483 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3912548" @default.
• W2113158483 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24309559" @default.
• W2113158483 hasPublicationYear "2013" @default.
• W2113158483 type Work @default.
• W2113158483 sameAs 2113158483 @default.
• W2113158483 citedByCount "40" @default.
• W2113158483 countsByYear W21131584832014 @default.
• W2113158483 countsByYear W21131584832015 @default.
• W2113158483 countsByYear W21131584832016 @default.
• W2113158483 countsByYear W21131584832017 @default.
• W2113158483 countsByYear W21131584832018 @default.
• W2113158483 countsByYear W21131584832019 @default.
• W2113158483 countsByYear W21131584832020 @default.
• W2113158483 countsByYear W21131584832021 @default.
• W2113158483 countsByYear W21131584832022 @default.
• W2113158483 crossrefType "journal-article" @default.
• W2113158483 hasAuthorship W2113158483A5034523396 @default.
• W2113158483 hasAuthorship W2113158483A5039686326 @default.
• W2113158483 hasAuthorship W2113158483A5039936196 @default.
• W2113158483 hasAuthorship W2113158483A5045765971 @default.
• W2113158483 hasAuthorship W2113158483A5048058203 @default.
• W2113158483 hasAuthorship W2113158483A5054584608 @default.
• W2113158483 hasAuthorship W2113158483A5064767923 @default.
• W2113158483 hasAuthorship W2113158483A5080630073 @default.
• W2113158483 hasAuthorship W2113158483A5081069263 @default.
• W2113158483 hasAuthorship W2113158483A5086342318 @default.
• W2113158483 hasBestOaLocation W21131584832 @default.
• W2113158483 hasConcept C104317684 @default.
• W2113158483 hasConcept C118131993 @default.
• W2113158483 hasConcept C126322002 @default.
• W2113158483 hasConcept C134018914 @default.
• W2113158483 hasConcept C167734588 @default.
• W2113158483 hasConcept C170493617 @default.
• W2113158483 hasConcept C17991360 @default.
• W2113158483 hasConcept C203014093 @default.
• W2113158483 hasConcept C2775960820 @default.
• W2113158483 hasConcept C2777025900 @default.
• W2113158483 hasConcept C2777077863 @default.

• next