53 research outputs found
Faecalibacterium prausnitzii prevents physiological damages in a chronic low-grade inflammation murine model
Cellular and molecular mechanism of interleukin-1β modulation of Caco-2 intestinal epithelial tight junction barrier.
P071 MECHANISM OF MMP-9 ACTIVATION OF MYOSIN LIGHT CHAIN KINASE (MLCK) MEDIATED DISRUPTION OF INTESTINAL TIGHT JUNCTION BARRIER
139 - Mechanism of MMP-9 Activation of Myosin Light Chain Kinase (MLCK) Mediated Disruption of Intestinal Tight Junction Barrier
M1785 Mechanism of Interleukin-1β Modulation of Intestinal Epithelial Barrier: Role of ERK1/2 Signaling Pathway and Elk-1
Tu1211 Interleukin-1beta (IL-1β) Induced Increase in Intestinal Epithelial Tight Junction Permeability (in-Vivo Is Mediated by ERK1/2 Signaling Pathway
200 Molecular Mechanism of IL-1β-Induced Increase in CACO-2 Intestinal Epithelial Tight Junction Permeability
Su1902 MMP-12 Modulation of Intestinal Epithelial Tight Junction Barrier Is Mediated by P38 Kinase Activation of Myosin Light Chain Kianse (MLCK)
Cellular and molecular mechanism of interleukin-1β modulation of Caco-2 intestinal epithelial tight junction barrier.
Interleukin-1β (IL-1β) is a prototypical multifunctional cytokine that plays an important role in intestinal inflammation of Crohn's disease and other inflammatory conditions of the gut. Previous studies have shown that IL-1β causes an increase in intestinal epithelial tight junction (TJ) permeability both in in vivo animal and in vitro cell culture model systems. The IL-1β-induced increase in intestinal epithelial TJ permeability has been postulated to be an important pathogenic mechanism contributing to intestinal inflammation. However, the signalling pathways and the molecular processes that mediate the IL-1β modulation of intestinal epithelial TJ barrier remain unclear. Here, we show that the IL-1β-induced increase in Caco-2 monolayer TJ permeability was mediated by activation of extracellular signal-regulated kinases 1/2 (ERK1/2) signalling pathway and that inhibition of ERK1/2 activity inhibits the IL-1β-induced increase in Caco-2 TJ permeability. The activation of ERK1/2 pathway caused a downstream activation of nuclear transcription factor Elk-1. The activated Elk-1 translocated to the nucleus and binds to the cis-binding motif on myosin light chain kinase (MLCK) promoter region, triggering MLCK gene activation, MLCK mRNA transcription and MLCK protein synthesis and MLCK catalysed opening of the intestinal epithelial TJ barrier. These studies provide novel insight into the cellular and molecular processes that mediate the IL-1β-induced increase in intestinal epithelial TJ permeability
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