scholarly journals Histidine deficiency attenuates cell viability in rat intestinal epithelial cells by apoptosis via mitochondrial dysfunction

2017 ◽  
Vol 8 ◽  
pp. 21-28 ◽  
Author(s):  
Tatsunobu Matsui ◽  
Hiroshi Ichikawa ◽  
Tomoka Fujita ◽  
Tomohisa Takagi ◽  
Mayuko Osada-Oka ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cell Viability ◽  
Mitochondrial Dysfunction ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial

scholarly journals CFTR Deletion Confers Mitochondrial Dysfunction and Disrupts Lipid Homeostasis in Intestinal Epithelial Cells

Nutrients ◽  
2018 ◽  
Vol 10 (7) ◽  
pp. 836 ◽  
Author(s):  
Marie Kleme ◽  
Alain Sané ◽  
Carole Garofalo ◽  
Ernest Seidman ◽  
Emmanuelle Brochiero ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mitochondrial Dysfunction ◽  
Intestinal Epithelial Cells ◽  
Lipid Homeostasis ◽  
Intestinal Epithelial

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.

scholarly journals Tumor Necrosis Factor-α and Apoptosis Signal-Regulating Kinase 1 Control Reactive Oxygen Species Release, Mitochondrial Autophagy and C-Jun N-Terminal Kinase/P38 Phosphorylation During Necrotizing Enterocolitis

2009 ◽  
Vol 2 (5) ◽  
pp. 297-306 ◽  
Author(s):  
Naira Baregamian ◽  
Jun Song ◽  
C. Eric Bailey ◽  
John Papaconstantinou ◽  
B. Mark Evers ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Mitochondrial Dysfunction ◽  
Tumor Necrosis ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial Cells ◽  
Oxygen Species ◽  
Intestinal Epithelial ◽  
Epithelial Cell Apoptosis ◽  
Necrosis Factor

Background: Oxidative stress and inflammation may contribute to the disruption of the protective gut barrier through various mechanisms; mitochondrial dysfunction resulting from inflammatory and oxidative injury may potentially be a significant source of apoptosis during necrotizing enterocolitis (NEC). Tumor necrosis factor (TNF)α is thought to generate reactive oxygen species (ROS) and activate the apoptosis signal-regulating kinase 1 (ASK1)-c-Jun N-terminal kinase (JNK)/p38 pathway. Hence, the focus of our study was to examine the effects of TNFα/ROs on mitochondrial function, ASK1-JNK/p38 cascade activation in intestinal epithelial cells during NEC.Results: We found (a) abundant tissue TNFα and ASK1 expression throughout all layers of the intestine in neonates with NEC, suggesting that TNFα/ASK1 may be a potential source (indicators) of intestinal injury in neonates with NEC; (b) TNFα-induced rapid and transient activation of JNK/p38 apoptotic signaling in all cell lines suggests that this may be an important molecular characteristic of NEC; (c) TNFα-induced rapid and transient ROs production in RIe-1 cells indicates that mitochondria are the predominant source of ROS, demonstrated by significantly attenuated response in mitochondrial DNA-depleted (RIE-1-ρ°) intestinal epithelial cells; (d) further studies with mitochondria-targeted antioxidant PBN supported our hypothesis that effective mitochondrial ROS trapping is protective against TNFα/ROs-induced intestinal epithelial cell injury; (e) TNFα induces significant mitochondrial dysfunction in intestinal epithelial cells, resulting in increased production of mtROS, drop in mitochondrial membrane potential (MMP) and decreased oxygen consumption; (f) although the significance of mitochondrial autophagy in NEC has not been unequivocally shown, our studies provide a strong preliminary indication that TNFα/ROs-induced mitochondrial autophagy may play a role in NeC, and this process is a late phenomenon.Methods: Paraffin-embedded intestinal sections from neonates with NEC and non-inflammatory condition of the gastrointestinal tract undergoing bowel resections were analyzed for TNFα and ASK1 expression. Rat (RIE-1) and mitochondrial DNA-depleted (RIE-1-ρ°) intestinal epithelial cells were used to determine the effects of TNFα on mitochondrial function.Conclusions: Our findings suggest that TNFα induces significant mitochondrial dysfunction and activation of mitochondrial apoptotic responses, leading to intestinal epithelial cell apoptosis during NeC. Therapies directed against mitochondria/ROS may provide important therapeutic options, as well as ameliorate intestinal epithelial cell apoptosis during NeC.

scholarly journals Alkaline Reduced Water Attenuates Oxidative Stress-Induced Mitochondrial Dysfunction and Innate Immune Response Triggered by Intestinal Epithelial Dysfunction

Processes ◽  
2021 ◽  
Vol 9 (10) ◽  
pp. 1828
Author(s):  
Jayson M. Antonio ◽  
Ailyn Fadriquela ◽  
Yun Ju Jeong ◽  
Cheol-Su Kim ◽  
Soo-Ki Kim
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Mitochondrial Dysfunction ◽  
Intestinal Epithelial Cells ◽  
Intestinal Barrier ◽  
Mapk Signaling ◽  
Raw 264.7 Cells ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Reduced Water

Redox imbalance in intestinal epithelial cells is critical in the early phases of intestinal injury. Dysfunction of the intestinal barrier can result in immunological imbalance and inflammation, thus leading to intestinal syndromes and associated illnesses. Several antioxidants have been discovered to be beneficial in resolving intestinal barrier dysfunction. Of these antioxidants, the effects of alkaline reduced water (ARW) in oxidative stress of intestinal epithelial cells and its immunokine modulation in vitro is unknown. In this study, we utilized ARW-enriched media to investigate its cytoprotective effect against H2O2-induced oxidative stress in DLD1 cells. We found that ARW rescued DLD1 from oxidative stress by diluting the influence of H2O2 on oxidative stress-activated MAPK signaling and mitochondrial dysfunction. Further, intestinal oxidative stress significantly affects immunokine profiles of Raw 264.7 cells (IL-6, IL-10, MCP, TNF-a, RANTES), which can be reversed by ARW. Collectively, ARW shields intestinal epithelial cells from oxidative stress, reducing the immunological mayhem caused by barrier failure.

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