FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1918150899> ?p ?o ?g. }

• W1918150899 endingPage "3185" @default.
• W1918150899 startingPage "3176" @default.
• W1918150899 abstract "Objective The NLRP3 inflammasome plays key roles in inflammation and autoimmunity, and purinergic receptor P2X 7 has been proposed to be upstream of NLRP3 activation. The aim of the present study, using murine models, was to investigate whether the P2X 7 /NLRP3 inflammasome pathway contributes to the pathogenesis of lupus nephritis (LN). Methods MRL/ lpr mice were treated with the selective P2X 7 antagonist brilliant blue G (BBG) for 8 weeks. Following treatment, the severity of renal lesions, production of anti–double‐stranded DNA (anti‐dsDNA) antibodies, rate of survival, activation of the NLRP3/ASC/caspase 1 inflammasome pathway, and ratio of Th17 cells to Treg cells were evaluated. P2X 7 ‐targeted small interfering RNA (siRNA) was also used for in vivo intervention. Similar evaluations were carried out in NZM2328 mice, a model of LN in which the disease was accelerated by administration of adenovirus‐expressing interferon‐α (AdIFNα). Results Significant up‐regulation of P2X 7 /NLRP3 inflammasome signaling molecules was detected in the kidneys of MLR/ lpr mice as compared with normal control mice. Blockade of P2X 7 activation by BBG suppressed NLRP3/ASC/caspase 1 assembly and the subsequent release of interleukin‐1β (IL‐1β), resulting in a significant reduction in the severity of nephritis and circulating anti‐dsDNA antibodies. The lifespan of the treated mice was significantly prolonged. BBG treatment reduced the serum levels of IL‐1β and IL‐17 and the Th17:Treg cell ratio. Similar results were obtained by specific siRNA silencing of P2X 7 in vivo. The effectiveness of BBG treatment in modulating LN was confirmed in NZM2328 mice with AdIFNα‐accelerated disease. Conclusion Activation of the P2X 7 signaling pathway accelerates murine LN by activating the NLRP3/ASC/caspase 1 inflammasome, resulting in increased IL‐1β production and enhanced Th17 cell polarization. Thus, targeting of the P2X 7 /NLRP3 pathway should be considered as a novel therapeutic strategy in patients with lupus." @default.
• W1918150899 created "2016-06-24" @default.
• W1918150899 creator A5002785482 @default.
• W1918150899 creator A5003759585 @default.
• W1918150899 creator A5032874127 @default.
• W1918150899 creator A5038828439 @default.
• W1918150899 creator A5042220634 @default.
• W1918150899 creator A5047069839 @default.
• W1918150899 creator A5067321308 @default.
• W1918150899 creator A5076087464 @default.
• W1918150899 creator A5080930329 @default.
• W1918150899 creator A5082134776 @default.
• W1918150899 date "2013-11-27" @default.
• W1918150899 modified "2023-10-17" @default.
• W1918150899 title "P2X₇ Blockade Attenuates Murine Lupus Nephritis by Inhibiting Activation of the NLRP3/ASC/Caspase 1 Pathway" @default.
• W1918150899 cites W1495057561 @default.
• W1918150899 cites W1511331632 @default.
• W1918150899 cites W1547552531 @default.
• W1918150899 cites W1548518540 @default.
• W1918150899 cites W1551045512 @default.
• W1918150899 cites W1593521707 @default.
• W1918150899 cites W1824528611 @default.
• W1918150899 cites W1950836695 @default.
• W1918150899 cites W1968119819 @default.
• W1918150899 cites W1971508661 @default.
• W1918150899 cites W1986803467 @default.
• W1918150899 cites W2009394579 @default.
• W1918150899 cites W2012706589 @default.
• W1918150899 cites W2017938209 @default.
• W1918150899 cites W2019702139 @default.
• W1918150899 cites W2028606370 @default.
• W1918150899 cites W2039809796 @default.
• W1918150899 cites W2051742762 @default.
• W1918150899 cites W2054596587 @default.
• W1918150899 cites W2067144100 @default.
• W1918150899 cites W2070893803 @default.
• W1918150899 cites W2071522059 @default.
• W1918150899 cites W2074405732 @default.
• W1918150899 cites W2104986316 @default.
• W1918150899 cites W2106178007 @default.
• W1918150899 cites W2106393574 @default.
• W1918150899 cites W2113148752 @default.
• W1918150899 cites W2115946221 @default.
• W1918150899 cites W2122644092 @default.
• W1918150899 cites W2124302947 @default.
• W1918150899 cites W2125867015 @default.
• W1918150899 cites W2133761093 @default.
• W1918150899 cites W2145190952 @default.
• W1918150899 cites W2150092978 @default.
• W1918150899 cites W2150107812 @default.
• W1918150899 cites W2151372649 @default.
• W1918150899 cites W2154579584 @default.
• W1918150899 cites W2156346381 @default.
• W1918150899 cites W2165709201 @default.
• W1918150899 cites W2169694612 @default.
• W1918150899 cites W2171462621 @default.
• W1918150899 cites W4214677758 @default.
• W1918150899 doi "https://doi.org/10.1002/art.38174" @default.
• W1918150899 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4038356" @default.
• W1918150899 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24022661" @default.
• W1918150899 hasPublicationYear "2013" @default.
• W1918150899 type Work @default.
• W1918150899 sameAs 1918150899 @default.
• W1918150899 citedByCount "158" @default.
• W1918150899 countsByYear W19181508992012 @default.
• W1918150899 countsByYear W19181508992013 @default.
• W1918150899 countsByYear W19181508992014 @default.
• W1918150899 countsByYear W19181508992015 @default.
• W1918150899 countsByYear W19181508992016 @default.
• W1918150899 countsByYear W19181508992017 @default.
• W1918150899 countsByYear W19181508992018 @default.
• W1918150899 countsByYear W19181508992019 @default.
• W1918150899 countsByYear W19181508992020 @default.
• W1918150899 countsByYear W19181508992021 @default.
• W1918150899 countsByYear W19181508992022 @default.
• W1918150899 countsByYear W19181508992023 @default.
• W1918150899 crossrefType "journal-article" @default.
• W1918150899 hasAuthorship W1918150899A5002785482 @default.
• W1918150899 hasAuthorship W1918150899A5003759585 @default.
• W1918150899 hasAuthorship W1918150899A5032874127 @default.
• W1918150899 hasAuthorship W1918150899A5038828439 @default.
• W1918150899 hasAuthorship W1918150899A5042220634 @default.
• W1918150899 hasAuthorship W1918150899A5047069839 @default.
• W1918150899 hasAuthorship W1918150899A5067321308 @default.
• W1918150899 hasAuthorship W1918150899A5076087464 @default.
• W1918150899 hasAuthorship W1918150899A5080930329 @default.
• W1918150899 hasAuthorship W1918150899A5082134776 @default.
• W1918150899 hasBestOaLocation W19181508992 @default.
• W1918150899 hasConcept C104317684 @default.
• W1918150899 hasConcept C119056186 @default.
• W1918150899 hasConcept C126322002 @default.
• W1918150899 hasConcept C139964883 @default.
• W1918150899 hasConcept C150903083 @default.
• W1918150899 hasConcept C170493617 @default.
• W1918150899 hasConcept C185592680 @default.
• W1918150899 hasConcept C203014093 @default.
• W1918150899 hasConcept C207001950 @default.
• W1918150899 hasConcept C22615655 @default.

• next