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• W2072287005 abstract "The origin of inflammatory bowel disease (IBD) is unknown and likely to be multifactorial. Our laboratory has established that in human mucosal smooth muscle cells (M-SMCs), cellular stress induced by virus or the viral mimic double-stranded RNA (polyinosinic:polycytidylic acid [poly I:C]) increases cell surface hyaluronan (HA) deposition and the formation of long cable-like structures of HA that are important for leukocyte attachment. Since leukocyte accumulation and hyperplasia of the M-SMCs are characteristic pathological changes observed in IBD patients, and phosphatidylinositol-3-kinase (PI3K)/Akt signaling pathways play established roles in cell survival, we investigated whether this pathway is involved in this unique HA-mediated leukocyte attachment. Poly I:C-stimulated M-SMCs bind significantly more monocytic cells than untreated cells and this response was inhibited in a dose-dependent manner by treatment with the PI3K inhibitor, LY294002. Since Akt is a critical downstream regulator of PI3K, we investigated the phosphorylation status of Akt in M-SMCs after treatment with poly I:C for 1 h and found that Akt was phosphorylated, but the phosphorylated Akt band was undetectable in LY294002 plus poly I:C-treated cultures. Confocal microscopy of M-SMCs stained for HA revealed that HA cable formation after poly I:C treatment was abrogated by LY294002. These results demonstrate that poly I:C-stimulated M-SMCs phosphorylate Akt, produce HA cables, and promote HA-mediated leukocyte adhesion through a PI3K/Akt-dependent manner." @default.
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• W2072287005 date "2010-11-01" @default.
• W2072287005 modified "2023-09-26" @default.
• W2072287005 title "Inhibition of the Phosphatidylinositol-3-Kinase Pathway Abrogates Polyinosinic:Polycytidylic Acid–Stimulated Hyaluronan-Mediated Human Mucosal Smooth Muscle Cell Binding of U937 Monocytic Cells" @default.
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• W2072287005 doi "https://doi.org/10.1089/jir.2009.0061" @default.
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