Loss of the Tight Junction Protein ZO-1 in Dextran Sulfate Sodium Induced Colitis

2007 ◽  
Vol 140 (1) ◽  
pp. 12-19 ◽  
Author(s):  
Lisa S. Poritz ◽  
Kristian I. Garver ◽  
Cecelia Green ◽  
Leo Fitzpatrick ◽  
Francesca Ruggiero ◽  
...  
Keyword(s):  
Tight Junction ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Tight Junction Protein ◽  
Junction Protein

scholarly journals Probiotic Mixture Protects Dextran Sulfate Sodium-Induced Colitis by Altering Tight Junction Protein Expressions and Increasing Tregs

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Yingdi Zhang ◽  
Xiaojing Zhao ◽  
Yunjuan Zhu ◽  
Jingjing Ma ◽  
Haiqin Ma ◽  
...  
Keyword(s):  
Tight Junction ◽  
Peripheral Blood ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intestinal Inflammation ◽  
Experimental Colitis ◽  
Mucosal Barrier ◽  
Intestinal Damage ◽  
Protective Effects ◽  
Junction Protein

Bifico is a probiotic mixture containing Bifidobacterium, Lactobacillus acidophilus, and Enterococcus. Studies support that Bifico has a protective effect in experimental colitis (IL-10-deficient and TNBS) models and in patients with inflammatory bowel disease (IBD). However, the mechanism underlying the protective effects of this mixture of probiotic bacteria remains incompletely clear. Here, we investigated the effect of Bifico on intestinal inflammation. In an in vivo experiment, dextran sulfate sodium was used to induce colitis. Bifico treatment significantly attenuated the severity of colitis in this model. Bifico increased the expression of tight junction proteins (TJs). In addition, Bifico increased the number of Tregs, but reduced the number of total CD4+ T cells in the peripheral blood. Furthermore, the expression of colonic CD4 protein was decreased while the level of forkhead box P3 (Foxp3) was upregulated. These results suggested that Bifico exerts beneficial effects on experimental colitis by increasing the expressions of TJs, upregulating the number of Tregs, and reducing the total CD4+ T cell number in both colon and peripheral blood. The intestinal damage in the pretreated + treated-Bifico-colitis group was more severe than that in only the pretreated-Bifico-colitis group. This suggested that Bifico might aggravate intestinal damage when the mucosal barrier is impaired.

scholarly journals Polycystin-2 Activity Is Controlled by Transcriptional Coactivator with PDZ Binding Motif and PALS1-associated Tight Junction Protein

2010 ◽  
Vol 285 (44) ◽  
pp. 33584-33588 ◽  
Author(s):  
Kerstin Duning ◽  
Deike Rosenbusch ◽  
Marc A. Schlüter ◽  
Yuemin Tian ◽  
Karl Kunzelmann ◽  
...  
Keyword(s):  
Tight Junction ◽  
Tight Junction Protein ◽  
Binding Motif ◽  
Transcriptional Coactivator ◽  
Junction Protein

scholarly journals Endothelial-specific insulin receptor substrate-1 overexpression worsens neonatal hypoxic-ischemic brain injury via mTOR-mediated tight junction disassembly

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yi-Fang Tu ◽  
Si-Tse Jiang ◽  
Chi-Wu Chiang ◽  
Li-Ching Chen ◽  
Chao-Ching Huang
Keyword(s):  
Endothelial Cells ◽  
Brain Injury ◽  
Tight Junction ◽  
Insulin Receptor ◽  
Vascular Endothelial Cells ◽  
Tight Junction Protein ◽  
Insulin Receptor Substrate ◽  
Vascular Endothelial ◽  
Transgenic Rats ◽  
Junction Protein

AbstractHypoxic-ischemic (HI) encephalopathy is the major cause of mortality and disability in newborns. The neurovascular unit is a major target of acute and chronic brain injury, and therapies that protect simultaneously both neurons and vascular endothelial cells from neonatal HI injury are in demand. Insulin receptors and its key downstream molecule-insulin receptor substrate −1 (IRS-1) are potential neuroprotective targets and expressed both in neuron and endothelial cells. To investigate whether IRS-1 can act similarly in neurons and vascular endothelial cells in protecting neurovascular units and brain form HI injury, we found that neuron-specific IRS-1 transgenic rats showed reduced neurovascular injury and infarct volumes, whereas endothelial-specific IRS-1 transgenic rats showed increased blood-brain barrier (BBB) disruption and exaggerated neurovascular injury after neonatal HI brain injury. Endothelial-specific IRS-1 overexpression increased vascular permeability and disassembled the tight junction protein (zonula occludens-1) complex. Inhibition of mammalian target of rapamycin (mTOR) by rapamycin preserved tight junction proteins and attenuated BBB leakage and neuronal apoptosis after HI in the endothelial-specific IRS-1 transgenic pups. Together, our findings suggested that neuronal and endothelial IRS-1 had opposite effects on the neurovascular integrity and damage after neonatal HI brain injury and that endothelial IRS-1 worsens neurovascular integrity after HI via mTOR-mediated tight junction protein disassembly.

The Tight Junction Protein Cingulin Regulates Gene Expression and RhoA Signaling

2009 ◽  
Vol 1165 (1) ◽  
pp. 88-98 ◽  
Author(s):  
Sandra Citi ◽  
Serge Paschoud ◽  
Pamela Pulimeno ◽  
Francesco Timolati ◽  
Fabrizio De Robertis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tight Junction ◽  
Tight Junction Protein ◽  
Junction Protein ◽  
Rhoa Signaling

Changes in tight junction protein expression in intrinsic aging and photoaging in human skin in vivo

2016 ◽  
Vol 84 (1) ◽  
pp. 99-101 ◽  
Author(s):  
Seon-Pil Jin ◽  
Sang Bum Han ◽  
Yeon Kyung Kim ◽  
Elizabeth Eunkyung Park ◽  
Eun Jin Doh ◽  
...  
Keyword(s):  
Protein Expression ◽  
Tight Junction ◽  
Human Skin ◽  
Tight Junction Protein ◽  
Tight Junction Protein Expression ◽  
Junction Protein

scholarly journals Hyaluronan 35 kDa treatment protects mice from Citrobacter rodentium infection and induces epithelial tight junction protein ZO-1 in vivo

2017 ◽  
Vol 62 ◽  
pp. 28-39 ◽  
Author(s):  
Yeojung Kim ◽  
Sean P. Kessler ◽  
Dana R. Obery ◽  
Craig R. Homer ◽  
Christine McDonald ◽  
...  
Keyword(s):  
Tight Junction ◽  
Tight Junction Protein ◽  
Citrobacter Rodentium ◽  
Junction Protein ◽  
Epithelial Tight Junction
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