Oxidative stress contributes to accelerated development of the senescent phenotype in human peritoneal mesothelial cells exposed to high glucose

2007 ◽  
Vol 42 (5) ◽  
pp. 636-641 ◽  
Author(s):  
Krzysztof Książek ◽  
Andrzej Bręborowicz ◽  
Achim Jörres ◽  
Janusz Witowski
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Mesothelial Cells ◽  
Peritoneal Mesothelial Cells ◽  
Senescent Phenotype ◽  
Human Peritoneal Mesothelial Cells

scholarly journals Effect of β-(3,4-Dihydroxyphenyl) Lactic Acid on Oxidative Stress Stimulated by High Glucose Levels in Human Peritoneal Mesothelial Cells

2012 ◽  
Vol 40 (3) ◽  
pp. 943-953 ◽  
Author(s):  
H Zhang ◽  
J-W Wang ◽  
Y Xu ◽  
K Zhang ◽  
B Yi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lactic Acid ◽  
High Glucose ◽  
Mesothelial Cells ◽  
Time Dependent ◽  
Enzyme Linked Immunosorbent Assay ◽  
Peritoneal Mesothelial Cells ◽  
Protein Levels ◽  
Glucose Levels ◽  
Human Peritoneal Mesothelial Cells

OBJECTIVE: To investigate the effects of β-(3,4-dihydroxyphenyl)lactic acid on oxidative stress stimulated by high glucose levels in human peritoneal mesothelial cells (HPMCs) in vitro. METHODS: HPMCs were incubated with 100 mol/l glucose followed by 0.625 – 20 mg/ml β-(3,4-dihydroxyphenyl)lactic acid. Reactive oxygen species (ROS) were quantified by flow cytometry. Relative levels of fibronectin-1 (FN1), collagen-I α1 (COL1A1), endothelin-1 (EDN1) and haem oxygenase-1 (HMOX1) mRNA and protein were quantified by real-time reverse transcription—polymerase chain reaction and Western blotting, respectively. Absolute levels of FN1 and COLIA1 were quantified by enzyme-linked immunosorbent assay. RESULTS: β-(3,4-Dihydroxyphenyl)lactic acid significantly decreased ROS levels, and EDN1 mRNA and protein levels, in dose- and time-dependent manners. HMOX1 mRNA and protein levels were significantly increased by β-(3,4-dihydroxyphenyl)lactic acid in dose-dependent manners. COL1A1 and FN1 mRNA and protein levels were significantly decreased by β-(3,4-dihydroxyphenyl)lactic acid in dose- and time-dependent manners. CONCLUSIONS: β-(3,4-Dihydroxyphenyl)lactic acid inhibited oxidative stress and reversed increases in FN1 and COLIA1 induced by high glucose levels in HPMCs. This may contribute to a protective role in peritoneal fibrosis.

scholarly journals High glucose promotes TGF-β1 production by inducing FOS expression in human peritoneal mesothelial cells

2015 ◽  
Vol 20 (1) ◽  
pp. 30-38 ◽  
Author(s):  
Keiko Kokoroishi ◽  
Ayumu Nakashima ◽  
Shigehiro Doi ◽  
Toshinori Ueno ◽  
Toshiki Doi ◽  
...  
Keyword(s):  
High Glucose ◽  
Mesothelial Cells ◽  
Peritoneal Mesothelial Cells ◽  
Human Peritoneal Mesothelial Cells ◽  
Fos Expression ◽  
Tgf Β1

Possible Role of Hepatocyte Growth Factor in Regeneration of Human Peritoneal Mesothelial Cells

2005 ◽  
Vol 28 (2) ◽  
pp. 141-149 ◽  
Author(s):  
Y. Naiki ◽  
K. Matsuo ◽  
T. Matsuoka ◽  
Y. Maeda
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
High Glucose ◽  
Glucose Solution ◽  
Mesothelial Cells ◽  
Matrix Metalloproteinase 2 ◽  
High Concentration ◽  
Peritoneal Mesothelial Cells ◽  
Human Peritoneal Mesothelial Cells ◽  
Hepatocyte Growth

Human peritoneal mesothelial cells (HPMCs) play an important role in peritoneal functions. During long term peritoneal dialysis, it has been reported that HPMCs are damaged by high glucose solution via the signal of transforming growth factor (TGF)- ß1 produced by HPMCs. In this study, we focused on the effect of hepatocyte growth factor (HGF), known as an anti-fibrotic and anti-TGF-ß1 agent, on HPMCs damaged by high glucose solution. HPMCs were isolated from specimens of the omentum from nonuremic patients after informed consent had been obtained. After confirming adhesion for 6 hours, 100 μL of DMEM with 0.5%FCS were added at different concentrations (D-glucose; 6, 30mM) with or without HGF (10, 30, 100 ng/mL) for 48 hours. We examined the effects of a high concentration of glucose and then focused on following four critical points: 1) the production of HGF from HPMCs exposed to a high concentration of glucose, 2) the expression of c-Met on HPMCs, 3) the viability of those cells, and 4) matrix metalloproteinase-2 (MMP-2) and tissue inhibitors of metalloproteinase-2 (TIMP-2). The following significant changes are described herein: high glucose solution and TGF-ß1 i) decreased HGF production from HPMCs and ii) up-regulated expression of c-Met on HPMCs, and addition of HGF iii) restored viability of HPMCs damaged by glucose, iv) suppressed TGF-ß1 production by HGF, and v) induced up-regulation of MMP-2 and decreased TIMP-2 production by HPMCs. Levels of HGF decreased by high concentrations of glucose in the peritoneal cavity may induce the loss of HPMCs and thereby result in peritoneal fibrosis. These results suggest that HGF is an effective agent in the regeneration of peritoneal membrane damaged by high glucose solution.

EndothelinB Receptor Blocker Inhibits High Glucose-Induced Synthesis of Fibronectin in Human Peritoneal Mesothelial Cells

2006 ◽  
Vol 26 (3) ◽  
pp. 393-401 ◽  
Author(s):  
Miyuki Shimizu ◽  
Yoshitaka Ishibashi ◽  
Fumika Taki ◽  
Hideki Shimizu ◽  
Ichiro Hirahara ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Mrna Expression ◽  
Real Time ◽  
High Glucose ◽  
Mesothelial Cells ◽  
Peritoneal Fibrosis ◽  
Peritoneal Mesothelial Cells ◽  
Protein Levels ◽  
Human Peritoneal Mesothelial Cells

Background Long-term peritoneal dialysis using glucose-based dialysates is associated with peritoneal fibrosis. The object of this study was to investigate the hypothesis that endothelin (ET)-1, which is known to play an important role in various fibrotic diseases, may also be involved in peritoneal fibrosis using human peritoneal mesothelial cells (HPMC). Methods HPMC were cultured with 4% d- or l-glucose, or loaded with 10 nmol/L ET-1. In some experiments, the ETA receptor antagonist BQ-123, the ETB receptor antagonist BQ-788, and antioxidants 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (TEMPOL) and diphenyleneiodium chloride (DPI) were used. mRNA expression of ET-1, ETA receptor, ETB receptor, and fibronectin (FN) was analyzed by real-time polymerase chain reaction (real-time PCR). The protein levels for FN and ET-1 were measured by ELISA. CM-H2DCFDA-sensitive reactive oxygen species (ROS) were evaluated by flow cytometry. Results d-Glucose significantly induced mRNA expression of ET-1 and the ETB receptor but not the ETA receptor. FN production under high glucose conditions was inhibited by BQ-788. ET-1 directly stimulated HPMC to increase mRNA expression of FN and CM-H2DCFDA-sensitive ROS production. BQ-788, TEMPOL, and DPI inhibited mRNA expression of FN induced by ET-1. Conclusion The present study suggests that high-glucose-induced FN synthesis is mediated by the ET-1/ETB receptor pathway and, therefore, an ETB receptor antagonist may be useful in preventing FN production in HPMC.

Hydrogen Sulfide Ameliorates High-Glucose Toxicity in Rat Peritoneal Mesothelial Cells by Attenuating Oxidative Stress

2014 ◽  
Vol 126 (3) ◽  
pp. 157-165 ◽  
Author(s):  
Ying Lu ◽  
Huaying Shen ◽  
Xiaosong Shi ◽  
Sheng Feng ◽  
Zhi Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
High Glucose ◽  
Mesothelial Cells ◽  
Glucose Toxicity ◽  
Peritoneal Mesothelial Cells

scholarly journals Effect of Glucose on Intercellular Junctions of Cultured Human Peritoneal Mesothelial Cells

2000 ◽  
Vol 11 (11) ◽  
pp. 1969-1979
Author(s):  
TAKAFUMI ITO ◽  
NORIAKI YORIOKA ◽  
MASAO YAMAMOTO ◽  
KATSUKO KATAOKA ◽  
MICHIO YAMAKIDO
Keyword(s):  
Peritoneal Dialysis ◽  
High Glucose ◽  
Transforming Growth Factor ◽  
Intercellular Junctions ◽  
Neutralizing Antibody ◽  
Transforming Growth Factor Β ◽  
Mesothelial Cells ◽  
Peritoneal Mesothelial Cells ◽  
Peritoneal Dialysis Fluid ◽  
Human Peritoneal Mesothelial Cells

Abstract. During continuous ambulatory peritoneal dialysis, the peritoneum is directly and continuously exposed to unphysiologic peritoneal dialysis fluid; the resulting mesothelial damage has been suggested to cause loss of ultrafiltration and dialysis efficacy. The present study investigated the effect of a high glucose concentration on cultured human peritoneal mesothelial cells to clarify the cause of decreased dialysis efficacy during prolonged peritoneal dialysis. High glucose caused a concentration-dependent decrease in cell proliferation, damage to the intercellular junctions, and excess production of transforming growth factor-β (TGF-β). The levels of intercellular junctional proteins (ZO-1, E-cadherin, and β-catenin) were decreased, and immuno-staining by anti—ZO-1 and anti— β-catenin antibodies became weaker and often discontinuous along the cell contour. Mannitol had similar but weaker effects at the same osmolality, and an anti—TGF-β neutralizing antibody reduced the effects of high glucose. Therefore, these effects were induced not only by glucose itself but also by hyperosmolality and by a glucose-induced increase of TGF-β. These findings suggest that the peritoneal mesothelium is damaged by prolonged peritoneal dialysis using high glucose dialysate and that impairment of the intercellular junctions of peritoneal mesothelial cells by high glucose dialysate induces peritoneal hyperpermeability and a progressive reduction in dialysis efficacy.

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