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NDT Advance Access published online on June 3, 2008
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfn273
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


3,4-Dideoxyglucosone-3-ene as a mediator of peritoneal demesothelization

Beatriz Santamaría1, Alvaro C. Ucero1, Ana Reyero1, Rafael Selgas2, Marta Ruiz-Ortega3, Marina Catalán1, Jesús Egido1 and Alberto Ortiz1

1 Unidad de Diálisis, Fundación Jiménez Díaz, Universidad Autónoma de Madrid, Instituto Reina Sofía de Investigación Nefrológica, 2 Servicio de Nefrología, Hospital Universitario La Paz 3 Laboratorio de Nefrología Experimental y Patología vascular, Fundación Jiménez Díaz, Madrid, Spain

Correspondence and offprint requests to: Beatriz Santamaria, Unidad de Diálisis, Fundación Jiménez Díaz, Av. Reyes Católicos 2, 28040 Madrid, Spain. Tel: +34-91-5504940; Fax: +34-91-544-26-36; E-mail: bsantamaria{at}fjd.es



  Abstract

Background. The mesothelium contributes significantly to the functional, structural and homeostatic properties of the peritoneum. Bioincompatible peritoneal dialysis solutions contribute to mesothelial cell loss during chronic peritoneal dialysis. Cell death has been implicated in mesothelial cell loss, but the molecular mechanisms have not been adequately characterized. We now report the modulation of mesothelial cell death by the glucose degradation product 3,4-dideoxyglucosone-3-ene (3,4-DGE).

Methods. Human mesothelial cells were cultured from the effluents of stable dialysis patients. Apoptosis was quantified in cultured mesothelial cells and in peritoneal effluents. Confocal microscopy and inhibitors were used to assess molecular mechanisms.

Results. Peritoneal dialysis solutions with a high content of both glucose and glucose degradation products, but not those with low glucose degradation product content, induced mesothelial cell apoptosis and loss of cell viability in culture and in vivo. 3,4-DGE also induced mesothelial cell apoptosis. Apoptosis induced by peritoneal dialysis solutions and 3,4-DGE was associated with oligomerization of Bax at mitochondria and caspase activation. Bax antagonism prevented caspase activation, apoptosis and cell death. The pancaspase inhibitor zVAD was also protective.

Conclusion. 3,4-DGE and peritoneal dialysis solutions with a high content in glucose degradation products induce mesothelial cell apoptosis by a Bax-dependent mechanism. This could contribute to chronic demesothelization in peritoneal dialysis.

Keywords: apoptosis; bax; caspases; glucose degradation products; mesothelium peritoneal dialysis

Received for publication: 3. 9.07
Accepted in revised form: 18. 4.08


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B. Santamaria, A. C. Ucero, A. Benito-Martin, R. Selgas, M. Ruiz-Ortega, A. B. Sanz, J. Egido, and A. Ortiz
TAMING APOPTOSIS IN PERITONEAL DIALYSIS
Perit. Dial. Int., February 1, 2009; 29(Supplement_2): S45 - S48.
[Abstract] [Full Text] [PDF]


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