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• W2000653090 abstract "Excessive inflammation is a major cause of organ damage during sepsis. The elderly are highly susceptible to sepsis-induced organ injury. Sirt1 expression is reduced during aging. In the present study, we investigated the role of Sirt1, a histone deacetylase, in controlling inflammatory responses in a murine sepsis model induced by cecal ligation and puncture (CLP). We examined lung inflammatory signaling in inducible Sirt1 knockout (Sirt1 −/− ) mice and wild-type littermates (Sirt1 +/+ ) after CLP. Our results demonstrated that Sirt1 deficiency led to severe lung inflammatory injury. To further investigate molecular mechanisms of Sirt1 regulation of lung inflammatory responses in sepsis, we conducted a series of experiments to assess lung inflammasome activation after CLP. We detected increased lung inflammatory signaling including NF-κB, signal transducer and activator of transcription 3, and ERK1/2 activation in Sirt1 −/− mice after CLP. Furthermore, inflammasome activity was increased in Sirt1 −/− mice after CLP, as demonstrated by increased IL-1β and caspase-7 cleavage and activation. Aggravated inflammasome activation in Sirt1 −/− mice was associated with the increased production of lung proinflammatory mediators, including ICAM-1 and high-mobility group box 1, and further disruption of tight junctions and adherens junctions, as demonstrated by dramatic reduction of lung claudin-1 and vascular endothelial-cadherin expression, which was associated with the upregulation of matrix metallopeptidase 9 expression. In summary, our results suggest that Sirt1 suppresses acute lung inflammation during sepsis by controlling inflammasome activation pathway." @default.
• W2000653090 created "2016-06-24" @default.
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• W2000653090 date "2015-04-15" @default.
• W2000653090 modified "2023-10-16" @default.
• W2000653090 title "Sirt1 restrains lung inflammasome activation in a murine model of sepsis" @default.
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• W2000653090 doi "https://doi.org/10.1152/ajplung.00274.2014" @default.
• W2000653090 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4398874" @default.
• W2000653090 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25659903" @default.
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