Renal epithelial cell injury and its promoting role in formation of calcium oxalate monohydrate

2010 ◽  
Vol 16 (3) ◽  
pp. 405-416 ◽  
Author(s):  
Jian-Ming Ouyang ◽  
Xiu-Qiong Yao ◽  
Jin Tan ◽  
Feng-Xin Wang
Keyword(s):  
Epithelial Cell ◽  
Calcium Oxalate ◽  
Cell Injury ◽  
Calcium Oxalate Monohydrate ◽  
Renal Epithelial Cell ◽  
Epithelial Cell Injury

scholarly journals A monoclonal antibody (1F3) to human glomerular epithelial cells: A new marker for renal epithelial cell injury.

1996 ◽  
Vol 9 (2) ◽  
pp. 222-228
Author(s):  
Yuji Morimoto ◽  
Shoji Kagami ◽  
Kaname Okada ◽  
Kouji Yasutomo ◽  
Takashi Kuhara ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Injury ◽  
Renal Epithelial Cell ◽  
Glomerular Epithelial Cells ◽  
Epithelial Cell Injury

scholarly journals H19 promote calcium oxalate nephrocalcinosis-induced renal tubular epithelial cell injury via a ceRNA pathway

EBioMedicine ◽  
2019 ◽  
Vol 50 ◽  
pp. 366-378 ◽  
Author(s):  
Haoran Liu ◽  
Tao Ye ◽  
Xiaoqi Yang ◽  
Jianhe Liu ◽  
Kehua Jiang ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Calcium Oxalate ◽  
Cell Injury ◽  
Tubular Epithelial Cell ◽  
Renal Tubular Epithelial Cell ◽  
Renal Tubular ◽  
Epithelial Cell Injury

Effects of chloride channel inhibitors on H2O2-induced renal epithelial cell injury

2000 ◽  
Vol 278 (1) ◽  
pp. F83-F90 ◽  
Author(s):  
Xianmin Meng ◽  
W. Brian Reeves
Keyword(s):  
Lipid Peroxidation ◽  
Dna Damage ◽  
Cell Death ◽  
Epithelial Cell ◽  
Small Molecules ◽  
Cell Injury ◽  
Membrane Integrity ◽  
Atp Depletion ◽  
Renal Epithelial Cell ◽  
Epithelial Cell Injury

Oxidative stress contributes to renal epithelial cell injury in certain settings. Chloride influx has also been proposed as an important component of acute renal epithelial cell injury. The present studies examined the role of Cl− in H2O2-induced injury to LLC-PK1 renal epithelial cells. Exposure of LLC-PK1 cells to 1 mM H2O2 resulted in the following: depletion of intracellular ATP content; DNA damage; lipid peroxidation; and a loss of membrane integrity to both small molecules, e.g., trypan blue, and macromolecules, e.g., lactate dehydrogenase (LDH), and cell death. Substitution of Cl− by isethionate or the inclusion of certain Cl− channel blockers, e.g., diphenylamine-2-carboxylate (DPC), 5-nitro-2-(3-phenylpropylamino)· benzoate (NPPB), and niflumic acid, prevented the H2O2-induced loss of membrane integrity to LDH. In addition, the H2O2-induced loss of membrane integrity was prevented by raising the osmolality of the extracellular solutions, by depletion of cell ATP, and by inhibitors of volume-sensitive Cl− channels. However, these maneuvers did not prevent the H2O2-induced permeability to small molecules or H2O2-induced ATP depletion, DNA damage, lipid peroxidation, or cell death. These results support the view that volume-sensitive Cl− channels play a role in the progressive loss of cell membrane integrity during injury.

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