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Lipopolysaccharide-Induced Increase in Intestinal Epithelial Tight Permeability Is Mediated by Toll-Like Receptor 4/Myeloid Differentiation Primary Response 88 (MyD88) Activation of Myosin Light Chain Kinase Expression.
Abstract Lipopolysaccharides (LPSs) are a major component of the Gram-negative bacterial cell wall and play an important role in mediating intestinal inflammatory responses in inflammatory bowel disease. Although recent studies suggested that physiologically relevant concentrations of LPS (0 to 1 ng/mL) cause an increase in intestinal epithelial tight junction (TJ) permeability, the mechanisms that mediate an LPS-induced increase in intestinal TJ permeability remain unclear. Herein, we show that myosin light chain kinase (MLCK) plays a central role in the LPS-induced increase in TJ permeability. Filter-grown Caco-...
Source: The American Journal of Pathology - November 22, 2017 Category: Pathology Authors: Nighot M, Al-Sadi R, Guo S, Rawat M, Nighot P, Watterson MD, Ma TY Tags: Am J Pathol Source Type: research

Overexpression of microRNA-495 improves the intestinal mucosal barrier function by targeting STAT3 via inhibition of the JAK/STAT3 signaling pathway in a mouse model of ulcerative colitis
Publication date: Available online 12 October 2017 Source:Pathology - Research and Practice Author(s): Xian-Qun Chu, Jing Wang, Guang-Xiang Chen, Guan-Qi Zhang, De-Yong Zhang, Yong-Yan Cai We aim to investigate the role of microRNA-495 (miR-495) in the intestinal mucosal barrier by indirectly targeting signal transducer and activator of transcription 3 (STAT3) through the Janus kinase-signal transducer and activator of transcription (JAK)/STAT3 signaling pathway in a mouse model of ulcerative colitis (UC). BALB/c mice were selected for establishing a mice model of UC, and intestinal tissues of normal and UC mice were coll...
Source: Pathology Research and Practice - October 13, 2017 Category: Pathology Source Type: research

The suppressor of cytokine signaling SOCS1 promotes apoptosis of intestinal epithelial cells via p53 signaling in Crohn's Disease.
This study was designed to investigate whether SOCS1 has a role in the death of intestinal epithelial cells and intestinal injury. The results showed that the expression of SOCS1 increased in CD patients, and the expression of SOCS1, p-p53 and PUMA increased in mouse TNBS induced colitis model. Using IFN-γ treated HT-29 cells as an apoptotic model of intestinal epithelial cells in vitro, we confirmed that SOCS1 promoted apoptosis of intestinal epithelial cells by activating p53. In HT-29 cells which were treated with IFN-γ, the interaction between p53 and SOCS1 and phosphorylation of p53 was significantly higher than unt...
Source: Experimental and Molecular Pathology - May 24, 2016 Category: Pathology Authors: Cui X, Shan X, Qian J, Ji Q, Wang L, Wang X, Li M, Ding H, Liu Q, Chen L, Zhang D, Ni R Tags: Exp Mol Pathol Source Type: research

Vacuolar protein sorting 4B regulates apoptosis of intestinal epithelial cells via p38 MAPK in Crohn's disease.
In this study, we reported for the first time that VPS4B was over-expressed in intestinal epithelial cell (IECs) of patients with CD. In TNBS-induced mouse colitis models, we observed the up-regulation of VPS4B was accompanied with the elevated levels of IEC apoptotic markers (active caspase-3 and cleaved PARP) and phosphorylated p38 in colitis IECs. Co-localization of VPS4B and active caspase-3 in IECs of the TNBS group further indicated the possible involvement of VPS4B in IEC apoptosis. Employing the TNF-α-treated HT29 cells as an in vitro IEC apoptosis model, we confirmed the positive correlation of VPS4B with caspase...
Source: Experimental and Molecular Pathology - December 20, 2014 Category: Pathology Authors: Zhang D, Wang L, Yan L, Miao X, Gong C, Xiao M, Ni R, Tang Q Tags: Exp Mol Pathol Source Type: research

Death-Associated Protein Kinase Controls STAT3 Activity in Intestinal Epithelial Cells.
ider-Stock R Abstract The TNF-IL-6-STAT3 pathway plays a crucial role in promoting ulcerative colitis-associated carcinoma (UCC). To date, the negative regulation of STAT3 is poorly understood. Interestingly, intestinal epithelial cells of UCC in comparison to ulcerative colitis show high expression levels of anti-inflammatory death-associated protein kinase (DAPK) and low levels of pSTAT3. Accordingly, epithelial DAPK expression was enhanced in STAT3(IEC-KO) mice. To unravel a possible regulatory mechanism, we used an in vitro TNF-treated intestinal epithelial cell model. We identified a new function of DAPK in ...
Source: The American Journal of Pathology - March 1, 2013 Category: Pathology Authors: Chakilam S, Gandesiri M, Rau TT, Agaimy A, Vijayalakshmi M, Ivanovska J, Wirtz RM, Schulze-Luehrmann J, Benderska N, Wittkopf N, Chellappan A, Ruemmele P, Vieth M, Rave-Fränk M, Christiansen H, Hartmann A, Neufert C, Atreya R, Becker C, Steinberg P, Schn Tags: Am J Pathol Source Type: research