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- W4313343412 abstract "Abstract β-arrestins are scaffolding proteins recently implicated as negative regulators of Toll-like receptor-4 (receptor for lipopolysaccharide from gram-negative bacteria) signaling in macrophages and fibroblasts. Unexpectedly, we find that β-arrestin-1 (β-arr-1) and -2 knockout mice are protected from endotoxic shock and lethality. Consistent with this, LPS-induced inflammatory cytokine (IL-1β, IL-12p40, IL-4, IL-5 and IFNγ) levels in the plasma are markedly inhibited in both β-arr-1 and -2 knockout mice, compared to the wild types. To identify the possible mechanisms involved, we examined the effect of LPS-induced cytokine production in CD11b+ and CD11b- splenocytes. Both splenocyte populations from β-arr-2 knockout mice showed a marked decrease LPS-induced IL1-β, IL-12p40, IL-5 and IFNγ whereas these cytokines were inhibited in the β-arr-1 knockout only in the CD11b- cells, when compared to wild type splenocytes. Further experiments on the signaling pathways indicate that the role of β-arrestins is independent of MAPK and IκBα pathways in both splenocyte populations. Interestingly LPS-induced increase in histone acetyl transferase activity in the spleen is significantly inhibited in both β-arr-1 and -2 knockout mice, suggesting chromatin modification as one potential mechanism. Taken together, these results indicate that both β-arrestins have overlapping but non-redundant and cell-type-specific roles in regulating LPS-induced inflammatory cytokine production in vivo." @default.
- W4313343412 created "2023-01-06" @default.
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- W4313343412 date "2010-04-01" @default.
- W4313343412 modified "2023-09-28" @default.
- W4313343412 title "β-arrestins mediate lipopolysaccharide-induced inflammatory response and endotoxemia in mice (94.10)" @default.
- W4313343412 doi "https://doi.org/10.4049/jimmunol.184.supp.94.10" @default.
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