AIMS: To offer a condensed description of the modes of cell death and the involved mechanisms behind them as detected in the different layers of the peritoneal tissue during experimental and clinical, long-term peritoneal dialysis (PD). MAIN REMARKS: Several types of cell death have been observed in the mesothelial monolayer: apoptosis, anoikis, secondary necrosis, pure necrosis and mitotic catastrophe. Death of mesothelial cells exposed to glucose-enriched solutions derives mainly from a degree of oxidative insult leading to DNA damage, provoked by glucose itself and/or its degradation products. Use of icodextrin is associated with a higher degree of oxidative injury that also leads to genomic damage and consequently to cell death. Peritoneal leukocytes exposed to glucose-enriched PD solutions share the fate of mesothelial cells. Endothelial cells treated in vitro with high glucose concentrations have higher rates of apoptosis induced by a degree of oxidative stress. Endothelial apoptosis plays an important role in remodeling the vascular network, since this development has been observed at the beginning of neo-angiogenesis and at the branching and regression of microvessels of neoformation. Acute osmotic stress results in increased proportions of mesothelial cells dying in apoptosis, anoikis, secondary necrosis as well as in pure necrosis. After long-term exposure, cells apparently adapt to the new hypertonic environment even though the eventual presence of functional changes cannot be ruled out. CONCLUSIONS: All cells lining the peritoneal cavity or living near its immediate environment, exposed most of the time to nonphysiological fluids, undergo changes that lead to their death. This problem is behind the poor regenerative capabilities showed by the mesothelial monolayer, the microvascular changes that lead to neoangiogenesis, and, probably, to a defective response to peritoneal infection. Therapeutic modulation of apoptotic cell death could inhibit its progress. Since liberation of oxygen radicals is thereby causally involved in apoptosis, reduced levels of GDPs and/or use of antioxidants appear to be indicated in order to prevent mesothelial, endothelial cells and leukocyte death.
AIMS: To offer a condensed description of the modes of cell death and the involved mechanisms behind them as detected in the different layers of the peritoneal tissue during experimental and clinical, long-term peritoneal dialysis (PD). MAIN REMARKS: Several types of cell death have been observed in the mesothelial monolayer: apoptosis, anoikis, secondary necrosis, pure necrosis and mitotic catastrophe. Death of mesothelial cells exposed to glucose-enriched solutions derives mainly from a degree of oxidative insult leading to DNA damage, provoked by glucose itself and/or its degradation products. Use of icodextrin is associated with a higher degree of oxidative injury that also leads to genomic damage and consequently to cell death. Peritoneal leukocytes exposed to glucose-enriched PD solutions share the fate of mesothelial cells. Endothelial cells treated in vitro with high glucose concentrations have higher rates of apoptosis induced by a degree of oxidative stress. Endothelial apoptosis plays an important role in remodeling the vascular network, since this development has been observed at the beginning of neo-angiogenesis and at the branching and regression of microvessels of neoformation. Acute osmotic stress results in increased proportions of mesothelial cells dying in apoptosis, anoikis, secondary necrosis as well as in pure necrosis. After long-term exposure, cells apparently adapt to the new hypertonic environment even though the eventual presence of functional changes cannot be ruled out. CONCLUSIONS: All cells lining the peritoneal cavity or living near its immediate environment, exposed most of the time to nonphysiological fluids, undergo changes that lead to their death. This problem is behind the poor regenerative capabilities showed by the mesothelial monolayer, the microvascular changes that lead to neoangiogenesis, and, probably, to a defective response to peritoneal infection. Therapeutic modulation of apoptotic cell death could inhibit its progress. Since liberation of oxygen radicals is thereby causally involved in apoptosis, reduced levels of GDPs and/or use of antioxidants appear to be indicated in order to prevent mesothelial, endothelial cells and leukocyte death.
Authors: Christoph Brochhausen; Volker H Schmitt; Taufiek K Rajab; Constanze N E Planck; Bernhard Krämer; Christine Tapprich; Markus Wallwiener; Helmut Hierlemann; Heinrich Planck; C James Kirkpatrick Journal: J Mater Sci Mater Med Date: 2012-05-10 Impact factor: 3.896
Authors: Asher A Mendelson; Qiunong Guan; Irina Chafeeva; Gerald A da Roza; Jayachandran N Kizhakkedathu; Caigan Du Journal: Perit Dial Int Date: 2013 Jan-Feb Impact factor: 1.756
Authors: Georgios Boudouris; Ioannis I Verginadis; Yannis V Simos; Andreas Zouridakis; Vasilios Ragos; Spyridon Ch Karkabounas; Angelos M Evangelou Journal: Int Urol Nephrol Date: 2012-12-02 Impact factor: 2.370