Glycogen synthase kinase-3 beta inhibitor suppresses Porphyromonas gingivalis lipopolysaccharide-induced CD40 expression by inhibiting nuclear factor-kappa B activation in mouse osteoblasts

Molecular Immunology
Liu DieLiang Xing

Abstract

Bone-forming osteoblasts have been recently reported capable of expressing the critical co-stimulatory molecule CD40 upon exposure to bacterial infection, which supports the unappreciated role of osteoblasts in modulating bone inflammation. Recent studies highlight the anti-inflammatory potential of glycogen synthase kinase-3β (GSK-3β) inhibitors; however, their effect on osteoblasts remains largely unclear. In the present study, we showed that treatment with SB216763, a highly specific GSK-3β inhibitor, resulted in a dose-dependent decrease in the mRNA and protein expression of CD40, as well as production of pro-inflammatory cytokines IL-6, TNF-α and IL-1β, in the Porphyromonas gingivalis-lipopolysaccharide (LPS)-stimulated murine osteoblastic-like MC3T3-E1 cells. Furthermore, inhibition of GSK-3β remarkably represses the LPS-induced activation of the nuclear factor kappa B (NF-κB) signaling pathway by suppressing IκBα phosphorylation, NF-κBp65 nuclear translocation, and NF-κBp65 DNA binding activity. Closer investigation by immunoprecipitation assay revealed that β-catenin can physically interact with NF-κBp65. The negative regulation effect of GSK-3β inhibitor on CD40 expression is mediated through β-catenin, for siRNA of β-...Continue Reading

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Feb 23, 2013·ISRN Endocrinology·Satoru MatsudaYasuko Kitagishi
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May 22, 2021·Frontiers in Immunology·Ricarda Cortés-VieyraVíctor M Baizabal-Aguirre

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