FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3025268019> ?p ?o ?g. }

• W3025268019 endingPage "129631" @default.
• W3025268019 startingPage "129631" @default.
• W3025268019 abstract "AMP-activated protein kinase (AMPK) exerts its anti-inflammatory effects by suppressing redox-sensitive nuclear factor kappa B (NF-κB) and pro-inflammatory cytokines including TNF-α. However, it is unclear whether AMPK regulates anti-inflammatory cytokine expressions in the presence of oxidative stress-induced inflammation. We sought to elucidate the mechanisms whereby AMPK regulates inflammatory cytokine expressions under NADPH oxidase (NOX)-induced oxidative stress. HT-29 human colonic epithelial cells transfected with AMPKα shRNA and mouse models with AMPKα knocked out in epithelial cells ( AMPKα fl/fl - Vil -Cre) or macrophages ( AMPKα fl/fl -Lyz2 -Cre) were used to examine the effects of AMPK and NOX on signaling pathways and cytokine expressions. In HT-29 cells, 5-hydroxytryptamine (5-HT)-induced NOX activity was enhanced by AMPKα silencing, and resulted in inflammatory cell death. AMPKα deletion specific for colon epithelial cells ( AMPKα fl/fl - Vil -Cre) or macrophages ( AMPKα fl/fl -Lyz2 -Cre) intensified 5-HT- or dextran sulfate sodium (DSS)-induced upregulations of NOX2, TNF-α, and IL-6, but completely abolished basal and 5-HT- or DSS-induced upregulation of IL-10 in colon epithelium. Furthermore, 5-HT- and DSS-induced changes were accompanied by marked upregulations of increased inflammatory signaling pathways linked to NF-κB, AP-1, and STAT3 transcription factors, and to GATA, a cell fate-directing signaling. In addition, AMPKα deletion significantly fortified 5-HT- or DSS-induced downregulations of cytoprotective signaling pathways (Nrf2, HIF-1α, and KLF4). Basal AMPKα maintains an anti-inflammatory state by inhibiting NOX, balancing pro−/anti-inflammatory signaling pathways, and directing IL-10 production. When these regulatory roles of AMPK are diminished by oxidative stress, colon epithelium undergoes inflammation despite IL-10 production. • Basal AMPKα maintains an anti-inflammatory state by inhibiting NOX. • AMPKα activity is inhibited by NOX2-mediated oxidative stress. • AMPKα deletion induces epithelial pyroptosis under oxidative stress. • AMPKα is essentially required for IL-10 expression. • AMPKα modulates crosstalk between Nrf2 and NF-κB in response to oxidative stress." @default.
• W3025268019 created "2020-05-21" @default.
• W3025268019 creator A5014039880 @default.
• W3025268019 creator A5024316231 @default.
• W3025268019 creator A5039805899 @default.
• W3025268019 creator A5046649612 @default.
• W3025268019 creator A5054654340 @default.
• W3025268019 creator A5055015781 @default.
• W3025268019 creator A5074466518 @default.
• W3025268019 creator A5076972824 @default.
• W3025268019 date "2020-08-01" @default.
• W3025268019 modified "2023-10-18" @default.
• W3025268019 title "AMPK is essential for IL-10 expression and for maintaining balance between inflammatory and cytoprotective signaling" @default.
• W3025268019 cites W1481874705 @default.
• W3025268019 cites W1504236935 @default.
• W3025268019 cites W1680789643 @default.
• W3025268019 cites W1856398487 @default.
• W3025268019 cites W1867120196 @default.
• W3025268019 cites W1899250089 @default.
• W3025268019 cites W1931329582 @default.
• W3025268019 cites W1941750967 @default.
• W3025268019 cites W1963632824 @default.
• W3025268019 cites W1964188773 @default.
• W3025268019 cites W1965694145 @default.
• W3025268019 cites W1971599078 @default.
• W3025268019 cites W1983428594 @default.
• W3025268019 cites W1989114351 @default.
• W3025268019 cites W1997745506 @default.
• W3025268019 cites W2004911892 @default.
• W3025268019 cites W2011093795 @default.
• W3025268019 cites W2013381549 @default.
• W3025268019 cites W2030845086 @default.
• W3025268019 cites W2039024936 @default.
• W3025268019 cites W2043043717 @default.
• W3025268019 cites W2043661379 @default.
• W3025268019 cites W2043880988 @default.
• W3025268019 cites W2049459709 @default.
• W3025268019 cites W2090321764 @default.
• W3025268019 cites W2093457368 @default.
• W3025268019 cites W2094615282 @default.
• W3025268019 cites W2104910525 @default.
• W3025268019 cites W2113794658 @default.
• W3025268019 cites W2123318646 @default.
• W3025268019 cites W2127351863 @default.
• W3025268019 cites W2128844539 @default.
• W3025268019 cites W2129224427 @default.
• W3025268019 cites W2133584350 @default.
• W3025268019 cites W2159235836 @default.
• W3025268019 cites W2164726701 @default.
• W3025268019 cites W2165528446 @default.
• W3025268019 cites W2171003762 @default.
• W3025268019 cites W2209250550 @default.
• W3025268019 cites W2319967189 @default.
• W3025268019 cites W2337416112 @default.
• W3025268019 cites W2399995528 @default.
• W3025268019 cites W2415939518 @default.
• W3025268019 cites W2555230408 @default.
• W3025268019 cites W2588368408 @default.
• W3025268019 cites W2590624416 @default.
• W3025268019 cites W2594664317 @default.
• W3025268019 cites W2730120915 @default.
• W3025268019 cites W2746079543 @default.
• W3025268019 cites W2767658071 @default.
• W3025268019 cites W2805029975 @default.
• W3025268019 cites W2884443157 @default.
• W3025268019 cites W2897080952 @default.
• W3025268019 cites W2897823504 @default.
• W3025268019 cites W2904955186 @default.
• W3025268019 cites W2905038699 @default.
• W3025268019 cites W2920889220 @default.
• W3025268019 doi "https://doi.org/10.1016/j.bbagen.2020.129631" @default.
• W3025268019 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32418902" @default.
• W3025268019 hasPublicationYear "2020" @default.
• W3025268019 type Work @default.
• W3025268019 sameAs 3025268019 @default.
• W3025268019 citedByCount "11" @default.
• W3025268019 countsByYear W30252680192020 @default.
• W3025268019 countsByYear W30252680192021 @default.
• W3025268019 countsByYear W30252680192022 @default.
• W3025268019 countsByYear W30252680192023 @default.
• W3025268019 crossrefType "journal-article" @default.
• W3025268019 hasAuthorship W3025268019A5014039880 @default.
• W3025268019 hasAuthorship W3025268019A5024316231 @default.
• W3025268019 hasAuthorship W3025268019A5039805899 @default.
• W3025268019 hasAuthorship W3025268019A5046649612 @default.
• W3025268019 hasAuthorship W3025268019A5054654340 @default.
• W3025268019 hasAuthorship W3025268019A5055015781 @default.
• W3025268019 hasAuthorship W3025268019A5074466518 @default.
• W3025268019 hasAuthorship W3025268019A5076972824 @default.
• W3025268019 hasConcept C164027704 @default.
• W3025268019 hasConcept C184235292 @default.
• W3025268019 hasConcept C185592680 @default.
• W3025268019 hasConcept C203014093 @default.
• W3025268019 hasConcept C2776914184 @default.
• W3025268019 hasConcept C2777730290 @default.
• W3025268019 hasConcept C2778690821 @default.
• W3025268019 hasConcept C2780124434 @default.
• W3025268019 hasConcept C62478195 @default.

• next