ArticleEuropean journal of medical research2026
Activated notch signaling pathway protects the intestinal barrier in DSS-induced colitis by regulating tight junctions.
Article in European journal of medical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
BACKGROUND AND
aimsStudies have suggested that the activation of Notch pathway may provide protection to the intestinal mucosal barrier. However, the underlying mechanism remains to be elucidated.
methodsIn vivo experiments, the dextran sulfate sodium (DSS)-induced colitis mice were used and LY411,575, a γ-secretase inhibitor, was orally administered for Notch signaling inhibition. In vitro experiments, we modulated Notch signaling by either activating or inhibiting it through the overexpression of Hes1 or LY411,575, respectively. The tight junction (TJ) and relevant myosin light chain kinase (MLCK) pathway were systematically investigated. To elucidate the mechanism underlying Notch activation, we conducted a comprehensive analysis of ligands and receptors associated with the Notch pathway in Caco-2 cells.
resultsCompared to DSS-colitis mice, inhibition of Notch activation by LY411,575 led to severe exacerbation of colitis, accompanied by TJ deterioration and concurrent activation of MLCK pathway. In vitro experiments confirmed the Notch signaling's regulatory effect on TJ function, with MLCK inhibitor ML-7 effectively mitigating the TJ dysfunction induced by LY411,575. Additionally, TNF-α-treated Caco-2 cells exhibited significantly increased expression of Jag1, Notch1, and Hes1. Silencing Jag1 using siRNA resulted in reduced NICD1 and Hes1 expression.
conclusionsActivation of Jag1/Notch1/Hes1 signaling pathway protects the intestinal mucosal barrier from inflammatory injury by abrogating MLCK-dependent TJ dysregulation.
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