Acute oxidative stress induces peritoneal hyperpermeability, mesothelial loss, and fibrosis

Gotloib, Lázaro; Wajsbrot, Valery; Cuperman, Yakov; Shostak, Avshalom

doi:10.1016/j.lab.2003.09.005

Cited by 44 publications

(35 citation statements)

References 41 publications

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“…Long-term peritoneal dialysis patients with peritoneal mesothelial cells exposed to high-glucose dialysate, low pH, lactate and GDP, and many other bioincompatible factors will be subject to injury and growth inhibition as well as extracellular matrix metabolism disorder (Linden et al 2001;Witowski et al 2001;Gotloib et al 2004). At the same time, peritoneal mesothelial cells might change into fibroblasts.…”

Section: Discussionmentioning

confidence: 99%

Epithelial–mesenchymal transition of rat peritoneal mesothelial cells via Rhoa/Rock pathway

Zhang

Liu

et al. 2010

In Vitro Cell.Dev.Biol.-Animal

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The objective of this study was to investigate the role of the RhoA/Rock signaling pathway in the epithelial-mesenchymal transition (EMT) of rat peritoneal mesothelial cells (RPMCs). Primary SD rat peritoneal mesothelial cells were cultured in vitro. RPMCs were randomly assigned to four groups: group A (control), group B (TGF-β1, 10 μg/L), group C (10 μg/L TGF-β1 + 10 μmol/L Y-27632, an inhibitor of Rock that was pre-applied for 2 h before TGF-β1 stimulation), and group D (Y-27632 alone, 10 μmol/L). Our results were as follows: (1) TGF-β1 stimulation elicited a robust increase in RhoA activity in a time-dependent manner; the increase was 2.57 ± 0.52 times larger than the activity observed for the control group (P < 0.05) after 10 min of stimulation. RhoA activity peaked at 1 h and was 4.35 ± 0.41 times the value observed for the control group (P < 0.05). (2) TGF-β1 up-regulated mRNA and/or protein expression of α-SMA, vimentin, and collagen and down-regulated mRNA and protein expression of E-cadherin in RPMCs. (3) The Rock inhibitor Y-27632 effectively reduced TGF-β1-induced expression of α-SMA, collagen, and vimentin; the mRNA levels of α-SMA and collagen decreased by 53.8% and 55.7%, respectively, and the protein levels of α-SMA, vimentin, and collagen decreased by 42.6%, 60.1%, and 58.1%, respectively, as compared to TGF-β1-stimulated groups (P < 0.05). However, the Rock inhibitor Y-27632 had no effect on the level of E-cadherin. In conclusion, the RhoA/Rock signaling pathway may mediate EMT induced by TGF-β1 in rat peritoneal mesothelial cells. The RhoA/Rock pathway may be a potential therapeutic target for the treatment of peritoneal fibrosis.

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Section: Discussionmentioning

confidence: 99%

Epithelial–mesenchymal transition of rat peritoneal mesothelial cells via Rhoa/Rock pathway

Zhang

Liu

et al. 2010

In Vitro Cell.Dev.Biol.-Animal

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“…This results in the localized release of inflammatory cytokines such as tumor necrosis factoralpha and interleukin-6 into the abdominal cavity, the subsequent recruitment of neutrophils, macrophages, and eosinophils, and the release of a fibrinous exudate into the peritoneum [1,2]. This process is associated with significant oxidative stress, both from the activation of the mesothelium and underlying endothelial cells and, more importantly, from the infiltration and subsequent activation of neutrophils and macrophages [3]. Ultimately, this inflammatory process leads to the formation of nascent, fibrinous adhesions.…”

Section: Introductionmentioning

confidence: 99%

Intraperitoneal Administration of Methylene Blue Attenuates Oxidative Stress, Increases Peritoneal Fibrinolysis, and Inhibits Intraabdominal Adhesion Formation

Heydrick

Reed

Cohen

et al. 2007

Journal of Surgical Research

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“…Overexpression of TGF-β1 driven by intraperitoneal adenovirus administration induced peritoneal fibrosis through epithelial mesenchymal transition, neoangiogenesis, and poor peritoneal function in mice [115][116][117][118] and rats [119,120]. Other chemical irritants, such as deoxycholate [121], household bleach [122] and acidic solutions [123], were also reported to produce peritoneal inflammation, fibrosis, and abdominal cocoon in rats.…”

Section: Zymosan-induced Fungal Peritonitis Modelmentioning

confidence: 99%

Peritonitis-induced peritoneal injury models for research in peritoneal dialysis review of infectious and non-infectious models

et al. 2017

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Peritonitis is an important complication of peritoneal dialysis. Several animal peritonitis models have been described, including bacterial and fungal models that are useful for studying inflammation in peritonitis. However, these models have limitations for investigating peritoneal fibrosis induced by acute inflammation and present difficulties in handling the infected animals. Animal models of peritonitis which induced peritoneal fibrosis are important for establishing new therapies to improve peritoneal damage induced by peritonitis. Here, we present an overview of representative animal models of peritoneal dialysis-associated infectious and non-infectious peritonitis, including our novel animal models (scraping and zymosan models) that mimic peritoneal injury associated with fibrosis and neoangiogenesis caused by bacterial or fungal peritonitis.

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Acute oxidative stress induces peritoneal hyperpermeability, mesothelial loss, and fibrosis

Cited by 44 publications

References 41 publications

Epithelial–mesenchymal transition of rat peritoneal mesothelial cells via Rhoa/Rock pathway

Epithelial–mesenchymal transition of rat peritoneal mesothelial cells via Rhoa/Rock pathway

Intraperitoneal Administration of Methylene Blue Attenuates Oxidative Stress, Increases Peritoneal Fibrinolysis, and Inhibits Intraabdominal Adhesion Formation

Peritonitis-induced peritoneal injury models for research in peritoneal dialysis review of infectious and non-infectious models

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