Effect of glucose peritoneal dialysates on the transmesothelial electrical resistance and cellular migration of monolayer human peritoneal mesothelial cell.
- Author:
Guanghui LING
1
;
Xuejing ZHU
;
Yuncheng XIA
;
Fuyou LIU
;
Youming PENG
;
Shaobin DUAN
;
Hong LIU
;
Yinghong LIU
;
Lin SUN
Author Information
1. Department of Nephrology, Second Xiangya Hospital, Central South University, Changsha 410011, China.
- Publication Type:Journal Article
- MeSH:
Cell Line;
Cell Membrane Permeability;
drug effects;
Cell Movement;
Electric Impedance;
Epithelium;
metabolism;
Glucose;
adverse effects;
metabolism;
Hemodialysis Solutions;
adverse effects;
Humans;
Peritoneal Dialysis;
Peritoneum;
cytology;
drug effects;
metabolism
- From:
Journal of Central South University(Medical Sciences)
2009;34(5):418-424
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect of different concentrations of glucose peritoneal dialysates (PDS) on monolayer transmesothelial electrical resistance (TER) and migration ability of cultured human peritoneal mesothelial cells (HPMCs) to clarify the cause of peritoneal hyperpermeability state and ultrafiltration failure during prolonged peritoneal dialysis.
METHODS:HPMCs were cultured in a 1:1 mixture of DMEM and PDS containing 1.5%, 2.5%, and 4.25% glucose. Methyl thiazolyl tetrazolium (MTT) assay and TER were measured to determine the effect of glucose PDS on the proliferation and permeability of human peritoneal mesothelial monolayers, respectively. Wound-healing assay was used to confirm whether glucose could do harm to the migration of cells.
RESULTS:Proliferation of HPMCs was significantly suppressed by different glucose concentrations at 24 hours. TER decreased in a time- and concentration-dependent manner after culture with different concentrations of glucose PDS. Cells lost migration in the presence of high glucose after 24 hours, and most cells lost their normal morphology and became detached from plates after 48 hours of wounding.
CONCLUSION:High glucose in PDS can cause peritoneal damage by suppressing cell proliferation, inducing increase in paracellular permeability of HPMCs and inhibiting cell migration after damage, which may be responsible for peritoneal hyperpermeability and the development of ultrafiltration failure.
