scholarly journals Trefoil factor 3 (TFF3) from human breast milk activates PAR-2 receptors, of the intestinal epithelial cells HT-29, regulating cytokines and defensins

2016 ◽  
Vol 117 (06) ◽  
pp. 332-339 ◽  
Author(s):  
G. J. Barrera ◽  
G. Sanchez Tortolero
Keyword(s):  
Breast Milk ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Human Breast Milk ◽  
Intestinal Epithelial ◽  
Trefoil Factor ◽  
Human Breast ◽  
Trefoil Factor 3 ◽  
Ht 29

scholarly journals Human breast milk-derived exosomes attenuate cell death in intestinal epithelial cells

2018 ◽  
Vol 24 (5) ◽  
pp. 278-284 ◽  
Author(s):  
Colin Martin ◽  
Mikita Patel ◽  
Sparkle Williams ◽  
Hamish Arora ◽  
Brian Sims
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Breast Milk ◽  
Epithelial Cells ◽  
Protective Effect ◽  
Cell Viability ◽  
Intestinal Epithelial Cells ◽  
Human Breast Milk ◽  
Intestinal Epithelial ◽  
Human Breast

Human breast milk has been shown to reduce the incidence of necrotizing enterocolitis (NEC). Breast milk has many components (immunoglobulins, proteins, fat, and, of recent interest, exosomes), but the specific component that affords protection against NEC is not known. Exosomes are small-nanometer vesicles that are rich in protein, lipid, and microRNA. Here, we hypothesized that human breast milk-derived exosomes can protect intestinal epithelial cells (IECs) from cell death. Human breast milk was collected, separated using ultracentrifugation, and quantified using NanoSight tracking analysis. Purified exosomes were added to IECs that had been treated with varying concentrations of H2O2. Cells were then incubated overnight with the human breast milk-derived exosomes and assessed for cell viability. Western blot analysis showed that both clathrin and CD81 were present in the purified sample. Oxidative stress using H2O2 caused a 50% decrease in cell viability and human breast milk-derived exosomes had a protective effect in IECs. In the presence of H2O2, exosomes had a statistically significant protective effect. The protection seen by human breast milk-derived exosomes was not attenuated by cycloheximide. Thus, human breast milk-derived exosomes allow IECs to be protected from oxidative stress, but the mechanism is still not clear. Exosomes derived from human breast milk are an attractive treatment concept for children with intestinal injury.

JAK/STAT3 Pathway in Human Intestinal Epithelial Cells During Trefoil Factor 3(TFF3) Mediated Cell Migration

2020 ◽  
Vol 17 (8) ◽  
pp. 993-1000
Author(s):  
Mengmeng Zhuang ◽  
Juan Le ◽  
Bo Zhu ◽  
Wenwen Zhang ◽  
Hao Yan ◽  
...  
Keyword(s):  
Cell Migration ◽  
Epithelial Cells ◽  
Matrix Metalloproteinases ◽  
Intestinal Epithelial Cells ◽  
The Body ◽  
Intestinal Epithelial ◽  
Trefoil Factor ◽  
Stat3 Pathway ◽  
Ht 29 ◽  
E Cadherin

Objective: Trefoil factor family is expressed in several tissues of the body and provides gastric and intestinal protection and healing. This research aims to indicate the mechanism involved in its function. Methods: The intestinal epithelial cells were pretreated with JAK inhibitor AG490 or the concentration of 60ug/ml human recombinant trefoil factor, while the levels of phospho-STAT3, E-cadherin and N-cadherin were detected by Western Blotting. The levels of Matrix Metalloproteinases, Ecadherin and N-cadherin were evaluated by quantitative real time PCR. The cell migration was assessed by the transwell assay and the scratch assay. The immunofluorescence method was performed to detect the reduction of molecular E-cadherin. Results: hTFF3 activates the JAK/STAT3 pathway in HT-29 cells. The effect of JAK/STAT3 pathway mechanism on cell migration promoted by hTFF3. TFF3 promoting cell migration is associated with increased gene transcription of MMPs. hTFF3 alters E-cadherin expression. hTFF3 activates the expression of N-cadherin and down-regulates E-cadherin expression in HT-29 Cells. Conclusion: We have shown that TFF3 activated the JAK/STAT3 pathway. TFF3 increased the level of Matrix Metalloproteinases and N-cadherin, decreased that of E-cadherin, while AG490 had the opposite effect. TFF3 accelerated cell migration and the AG490 relieved the migrating rate to control the levels. TFF3 activated JAK/STAT3 pathway which was associated with intestinal epithelial cell migration.

scholarly journals TFF3 modulates NF-κB and a novel negative regulatory molecule of NF-κB in intestinal epithelial cells via a mechanism distinct from TNF-α

2005 ◽  
Vol 289 (5) ◽  
pp. C1085-C1093 ◽  
Author(s):  
Ya-Qin Zhu ◽  
Xiao-Di Tan
Keyword(s):  
Tumor Necrosis Factor ◽  
Epithelial Cells ◽  
Tumor Necrosis ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Trefoil Factor ◽  
Trefoil Factor 3 ◽  
Twist Protein ◽  
Factor Α ◽  
Necrosis Factor

Trefoil factor 3 (intestinal trefoil factor) is a cytoprotective factor in the gut. Herein we compared the effect of trefoil factor 3 with tumor necrosis factor-α on 1) activation of NF-κB in intestinal epithelial cells; 2) expression of Twist protein (a molecule essential for downregulation of nuclear factor-κB activity in vivo); and 3) production of interleukin-8. We showed that Twist protein is constitutively expressed in intestinal epithelial cells. Tumor necrosis factor-α induced persistent degradation of Twist protein in intestinal epithelial cells via a signaling pathway linked to proteasome, which was associated with prolonged activation of NF-κB. In contrast to tumor necrosis factor, trefoil factor 3 triggered transient activation of NF-κB and prolonged upregulation of Twist protein in intestinal epithelial cells via an ERK kinase-mediated pathway. Unlike tumor necrosis factor-α, transient activation of NF-κB by trefoil factor 3 is not associated with induction of IL-8 in cells. To examine the role of Twist protein in intestinal epithelial cells, we silenced the Twist expression by siRNA. Our data showed that trefoil factor 3 induced interleukin-8 production after silencing Twist in intestinal epithelial cells. Together, these observations indicated that 1) trefoil factor 3 triggers a diverse signal from tumor necrosis factor-α on the activation of NF-κB and its associated molecules in intestinal epithelial cells; and 2) trefoil factor 3-induced Twist protein plays an important role in the modulation of inflammatory cytokine production in intestinal epithelial cells.

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