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• W4311556918 startingPage "e0278910" @default.
• W4311556918 abstract "Macrophages play a crucial role in inflammation, a defense mechanism of the innate immune system. Metabolic function powered by glucose transporter isoform 1 (Glut1) is necessary for macrophage activity during inflammation. The present study investigated the roles of cystathionine-γ-lyase (CSE) and its byproduct, hydrogen sulfide (H 2 S), in macrophage glucose metabolism to explore the mechanism by which H 2 S acts as an inflammatory regulator in lipopolysaccharide- (LPS) induced macrophages. Our results demonstrated that LPS-treated macrophages increased Glut1 expression. LPS-induced Glut1 expression is regulated via nuclear factor (NF)-κB activation and is associated with phosphatidylinositol-3-kinase PI3k activation. Small interfering (si) RNA-mediated silencing of CSE decreased the LPS-induced NF-κB activation and Glut1 expression, suggesting a role for H 2 S in metabolic function in macrophages during pro-inflammatory response. Confoundingly, treatment with GYY4137, an H 2 S-donor molecule, also displayed inhibitory effects upon LPS-induced NF-κB activation and Glut1 expression. Moreover, GYY4137 treatment increased Akt activation, suggesting a role in promoting resolution of inflammation. Our study provides evidence that the source of H 2 S, either endogenous (via CSE) or exogenous (via GYY4137), supports or inhibits the LPS-induced NF-κB activity and Glut1 expression, respectively. Therefore, H 2 S may influence metabolic programming in immune cells to alter glucose substrate availability that impacts the immune response." @default.
• W4311556918 created "2022-12-27" @default.
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• W4311556918 date "2022-12-15" @default.
• W4311556918 modified "2023-10-01" @default.
• W4311556918 title "Cystathionine γ-lyase and hydrogen sulfide modulates glucose transporter Glut1 expression via NF-κB and PI3k/Akt in macrophages during inflammation" @default.
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• W4311556918 doi "https://doi.org/10.1371/journal.pone.0278910" @default.
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