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NDT Advance Access originally published online on January 6, 2009
Nephrology Dialysis Transplantation 2009 24(6):1799-1809; doi:10.1093/ndt/gfn718
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© The Author [2009]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Heat shock response protects human peritoneal mesothelial cells from dialysate-induced oxidative stress and mitochondrial injury

Hung-Tien Kuo1,2, Hsiang-Wen Chen3, Hui-Hsu Hsiao3 and Hung-Chun Chen1,2

1 Division of Nephrology, Department of Internal Medicine, Kaohsiung Medical University Hospital 2 Faculty of Renal Care 3 Department of Microbiology, Faculty of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan

Correspondence and offprint requests to: Hung-Chun Chen; E-mail: chenhc{at}kmu.edu.tw



  Abstract

Background. Chronic peritoneal dialysis (PD) is one of the major therapies for uremic patients. However, the peritoneal mesothelial cells (PMCs) are subject to the injury by bioincompatible dialysates. The aim of this study is to investigate the protective roles and mechanisms of heat shock response in PMCs.

Methods. Primary cultured human PMCs (HPMCs) were subjected to commercial peritoneal dialysates. The cell viability was assayed by MTT test and Annexin V assay. The expression of HSPs was detected by Western blots analysis. Intracellular hydrogen peroxide and superoxide anion were detected using H2DCFDA and dHE probe, respectively, with flow cytometry. The mitochondrial membrane potential ({Delta}{Psi}m) of HPMCs was evaluated using JC1 probe with flow-cytometry.

Results. Exposure of HPMCs to 1.5%, 2.5%, and 4.25% dextrose, and 7.5% icodextrin dialysates, respectively, for 60 min resulted in significantly accumulation of intracellular reactive oxygen species (ROS), {Delta}{Psi}m loss, and cell death in HPMCs. Amino acid dialysates exhibited no significant cytotoxicity. Adjusting the acidity in 1.5% dextrose and icodextrin dialysate significantly attenuated the dialysate-induced ROS generation and cell death in HPMCs. Heat pretreatment (41°C, 30 minutes), which induced HSP 27 and 72 syntheses, significantly attenuated the dialysate-induced intracellular ROS accumulation, Dym loss, and cell death in HPMCs.

Conclusions. In conclusion, the acidic bioincompatible dialysates induce oxidative stress, {Delta}{Psi}m loss, and subsequent cell death in HPMCs. Amino acid dialysates is more biocompatible than glucose and icodextrin dialysates to HPMCs. Heat shock response protects HPMCs from the bioincompatible dialysates-induced cellular damage.

Keywords: heat shock protein; mitochondria; oxidative stress; peritoneal mesothelial cells

Received for publication: 30.10.07
Accepted in revised form: 28.11.08


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