Goose nephritic astrovirus infection increases autophagy, destroys intercellular junctions in renal tubular epithelial cells, and damages podocytes in the kidneys of infected goslings

2021 ◽  
pp. 109244
Author(s):  
Han Huang ◽  
Rui Ding ◽  
Zongyan Chen ◽  
Zewen Yi ◽  
Hongyu Wang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intercellular Junctions ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Renal Tubular

scholarly journals MiR-30c regulates cisplatin-induced apoptosis of renal tubular epithelial cells by targeting Bnip3L and Hspa5

2017 ◽  
Vol 8 (8) ◽  
pp. e2987-e2987 ◽  
Author(s):  
Bin Du ◽  
Xiao-meng Dai ◽  
Shuang Li ◽  
Guo-long Qi ◽  
Guang-xu Cao ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Renal Tubular ◽  
Induced Apoptosis

Cadmium and Molybdenum co-induce pyroptosis via ROS/PTEN/PI3K/AKT axis in duck renal tubular epithelial cells

2020 ◽  
pp. 116403
Author(s):  
Caiying Zhang ◽  
Tianjin Lin ◽  
Gaohui Nie ◽  
Ruiming Hu ◽  
Shaoxing Pi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Renal Tubular

Possible reason for preferential damage to renal tubular epithelial cells evoked by amphotericin B.

1996 ◽  
Vol 40 (5) ◽  
pp. 1116-1120 ◽  
Author(s):  
I Walev ◽  
S Bhakdi
Keyword(s):  
Epithelial Cells ◽  
Amphotericin B ◽  
Important Determinant ◽  
Major Complication ◽  
Toxic Action ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Recovery Mechanisms ◽  
Renal Tubular

An important determinant of nephrotoxicity, which is the major complication of long-term amphotericin B treatment, is dysfunction of distal tubular epithelial cells. The underlying cause for this rather selective damage to the cells is unknown. In the present investigation, it was shown that kidney epithelial cells were initially damaged by amphotericin B at concentrations of 2.5 to 10 micrograms/ml, as demonstrable by a dramatic drop in cellular K+ levels. Cells could recover from the initial toxic action of the polyene if they were kept in medium of neutral pH, and cellular K+ levels returned to normal after 6 h. However, the recovery mechanisms failed at lower pHs of 5.6 to 6.0. At low pHs, cells became progressively depleted of ATP; they leaked lactate dehydrogenase and became irreversibly damaged after approximately 6 h. The possibility that the low pH characteristic of the distal tubulus lumen renders the renal epithelial cells particularly vulnerable to the toxic action of amphotericin B is raised. The concept is in line with an earlier report that alkalization ameliorates amphotericin B nephrotoxicity in rats.

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