scholarly journals Human Peritoneal Mesothelial Cell Death Induced by High-Glucose Hypertonic Solution Involves Ca2+ and Na+ Ions and Oxidative Stress with the Participation of PKC/NOX2 and PI3K/Akt Pathways

2017 ◽  
Vol 8 ◽  
Author(s):  
Felipe Simon ◽  
Pablo Tapia ◽  
Ricardo Armisen ◽  
Cesar Echeverria ◽  
Sebastian Gatica ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
High Glucose ◽  
Mesothelial Cell ◽  
Hypertonic Solution ◽  
Na Ions ◽  
And Oxidative Stress ◽  
Peritoneal Mesothelial Cell ◽  
Human Peritoneal Mesothelial Cell

scholarly journals Involvement of STAT3 Signaling in High Glucose-Induced Epithelial Mesenchymal Transition in Human Peritoneal Mesothelial Cell Line HMrSV5

2019 ◽  
Vol 44 (2) ◽  
pp. 179-187 ◽  
Author(s):  
Pei Zhang ◽  
Hong Dai ◽  
Lei Peng
Keyword(s):  
Cell Line ◽  
High Glucose ◽  
Epithelial Mesenchymal Transition ◽  
Critical Role ◽  
Mesothelial Cell ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mesenchymal Transition ◽  
Stat3 Signaling ◽  
Peritoneal Mesothelial Cell ◽  
Human Peritoneal Mesothelial Cell

Background/Aims: Peritoneal fibrosis (PF) is a common complication in patients receiving long-term peritoneal dialysis, which results in damage to peritoneal functions. Epithelial-mesenchymal transition (EMT) is a key step in the early pathogenesis of PF. Increasing evidence has shown that signal transducer and activator of transcription 3 (STAT3) signaling pathway is involved in EMT and tissue fibrosis by interacting with distinct EMT-inducing molecules, including transforming growth factor (TGF)-β and advanced glycation end products (AGEs). This study investigated the involvement of STAT3 in the PF process. Methods: We used high glucose-treated human peritoneal mesothelial cell line HMrSV5 as an in vitro model to expose the peritoneal mesothelial cells to high-glucose dialysate. Expression of EMT markers was detected by qRT-PCR. Accumulation of methylglyoxal (MGO) and AGEs in the culture supernatant were measured by enzyme-linked immunosorbent assay. Phosphorylation of STAT3 was assessed by Western blot. Results: Results showed that high glucose upregulated TGF-β, increased the productions of MGO and AGEs, and induced EMT in HMrSV5 cells. High glucose also activated the STAT3 pathway. STAT3 inhibitor reduced the high glucose-induced EMT, via reducing TGF-β expression and repressing the accumulation of MGO and AGEs. Conclusion: Our results revealed a critical role for STAT3 signaling in high glucose-induced EMT in HMrSV5 cells, and suggested that inhibition of STAT3 might be a treatment for high glucose-induced fibrogenesis in PF.

scholarly journals Caspase-2 and oxidative stress underlie the immunogenic potential of high hydrostatic pressure-induced cancer cell death

2016 ◽  
Vol 6 (1) ◽  
pp. e1258505 ◽  
Author(s):  
Irena Moserova ◽  
Iva Truxova ◽  
Abhishek D. Garg ◽  
Jakub Tomala ◽  
Patrizia Agostinis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Hydrostatic Pressure ◽  
Cancer Cell ◽  
High Hydrostatic Pressure ◽  
Cancer Cell Death ◽  
Caspase 2 ◽  
And Oxidative Stress

scholarly journals TMIGD1 Inhibited Abdominal Adhesion Formation by Alleviating Oxidative Stress in the Mitochondria of Peritoneal Mesothelial Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Yunhua Wu ◽  
Enmeng Li ◽  
Zijun Wang ◽  
Tianli Shen ◽  
Cong Shen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Function ◽  
Adhesion Formation ◽  
Mesothelial Cell ◽  
Mesothelial Cells ◽  
Stress Injury ◽  
Peritoneal Mesothelial Cells ◽  
Abdominal Adhesion ◽  
Adhesion Tissue ◽  
Peritoneal Mesothelial Cell

Background. Postoperative abdominal adhesion remains one of the frequent complications after abdominal surgery and lacks effective intervention. Peritoneal mesothelial cell injury and healing play crucial roles in the process of adhesion formation, and identifying this mechanism might provide new insight into possible new therapeutic strategies for this disease. Transmembrane and immunoglobulin domain-containing 1 (TMIGD1) has been proven to protect renal epithelial cells from injury induced by oxidative stress and has also been identified as a novel adhesion molecule. Here, we investigated the role of TMIGD1 and its possible mechanism in adhesion formation. Materials and Methods. Immunohistochemistry (IHC), qPCR, and immunofluorescence (IHF) were used to detect the expression of TMIGD1. The grade and tenacity score of adhesion were used to evaluate the adhesion formation conditions. A TMIGD1-overexpressing HMrSV5 cell line was established. MTT assay, Western blotting, Annexin V apoptosis analysis, and CK19 staining were used to measure mesothelial cell viability, apoptosis, and completeness. ROS and MDA detection were used to measure mesothelial cell oxidative stress levels. JC-1 staining, IHF, and transmission electron microscopy were performed to assess mitochondrial function. Scratch-wound and adhesion assays were used to evaluate the adhesion ability of mesothelial cells. Results. First, we showed that TMIGD1 was decreased in mouse abdominal adhesion tissue and peritoneal mesothelial cells. Second, TMIGD1 overexpression inhibited adhesion formation. Third, TMIGD1 overexpression protected mesothelial cells from hydrogen peroxide- (H2O2-) induced oxidative stress injury. Fourth, TMIGD1 overexpression alleviated oxidative stress by protecting the mitochondrial function of mesothelial cells. In addition, TMIGD1 overexpression enhanced mesothelial cell adhesion. Conclusion. Our findings suggest that TMIGD1 protects mesothelial cells from oxidative stress injury by protecting their mitochondrial function, which is decreased in regular abdominal adhesion tissue. In addition, TMIGD1 enhances peritoneal mesothelial cell adhesion to promote healing.

scholarly journals Gain in toxic function of stefin B EPM1 mutants aggregates: Correlation between cell death, aggregate number/size and oxidative stress

2014 ◽  
Vol 1843 (9) ◽  
pp. 2089-2099 ◽  
Author(s):  
Mira Polajnar ◽  
Tina Zavašnik-Bergant ◽  
Nataša Kopitar-Jerala ◽  
Magda Tušek-Žnidarič ◽  
Eva Žerovnik
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
And Oxidative Stress
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