New insights into the mechanisms involved in renal proximal tubular damage induced in vitro by ochratoxin A

2004 ◽  
Vol 18 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Alessandra Gennari ◽  
Patricia Pazos ◽  
Monica Boveri ◽  
Robert Callaghan ◽  
Juan Casado ◽  
...  
Keyword(s):  
Ochratoxin A ◽  
Tubular Damage ◽  
Proximal Tubular ◽  
Proximal Tubular Damage ◽  
Renal Proximal Tubular

Transcriptomic alterations induced by Ochratoxin A in rat and human renal proximal tubular in vitro models and comparison to a rat in vivo model

2011 ◽  
Vol 86 (4) ◽  
pp. 571-589 ◽  
Author(s):  
Paul Jennings ◽  
Christina Weiland ◽  
Alice Limonciel ◽  
Katarzyna M. Bloch ◽  
Robert Radford ◽  
...  
Keyword(s):  
Ochratoxin A ◽  
In Vitro Models ◽  
In Vivo Model ◽  
Proximal Tubular ◽  
Renal Proximal Tubular

Urinary Trehalase Activity Is a Useful Marker of Renal Proximal Tubular Damage in Newborn Infants

Nephron ◽  
1995 ◽  
Vol 70 (4) ◽  
pp. 443-448 ◽  
Author(s):  
Misa Sasai-Takedatsu ◽  
Takatsugu Kojima ◽  
Shigeru Taketani ◽  
Atsushi Ono ◽  
Naoyuki Kitamura ◽  
...  
Keyword(s):  
Newborn Infants ◽  
Tubular Damage ◽  
Trehalase Activity ◽  
Proximal Tubular ◽  
Proximal Tubular Damage ◽  
Renal Proximal Tubular

In Vitro and In Vivo Evaluation of Amphiphilic Chitosan Derivatives for Inhibition of Organic Cation Transport Function

2020 ◽  
Vol 859 ◽  
pp. 45-50
Author(s):  
Sirima Soodvilai ◽  
Sunhapas Soodvila ◽  
Warayuth Sajomsang ◽  
Theerasak Rojanarata ◽  
Prasopchai Patrojanasophon ◽  
...  
Keyword(s):  
Organic Cation ◽  
Drug Disposition ◽  
Organic Cation Transporter ◽  
Transport Function ◽  
Chitosan Derivatives ◽  
Proximal Tubular Epithelial Cells ◽  
Proximal Tubular ◽  
Renal Proximal Tubular

This study explored the interaction of amphiphilic chitosan derivatives, N-benzyl-N,O-succinyl chitosan (BSCS), N-naphthyl-N,O-succinyl chitosan (NSCS) and N-octyl-N,O-succinyl chitosan (OSCS), with renal organic cation transporter 2 (OCT2). The influence of amphiphilic chitosan derivatives on renal OCT2 transport function was determined by monitoring the transport of a positively charged substrate into human renal proximal tubular epithelial cells (RPTEC/TERT1 cells), and murine kidney. Amphiphilic chitosan derivatives inhibited 3H-MPP (a substrate of OCT2) transport in the renal cells in a concentration-reliance characteristic. OSCS reduced the accumulation of the cationic drug, cisplatin, in RPTEC/TERT1 cells. This effect was more pronounced than that of other chitosan derivatives. In addition, co-administration of cisplatin and OSCS significantly reduced cisplatin accumulation compared with receiving cisplatin alone. This result was accompanied by the decrease in nephrotoxicity induced by cisplatin. In conclusion, OSCS inhibited OCT2 function and reduced cationic drug disposition in human renal proximal tubular cells and murine kidney.

scholarly journals Sodium Glucose Co-Transporter 2 Inhibitor Ameliorates Autophagic Flux Impairment on Renal Proximal Tubular Cells in Obesity Mice

2020 ◽  
Vol 21 (11) ◽  
pp. 4054
Author(s):  
Kazuhiko Fukushima ◽  
Shinji Kitamura ◽  
Kenji Tsuji ◽  
Yizhen Sang ◽  
Jun Wada
Keyword(s):  
Renal Injury ◽  
Tubular Damage ◽  
Autophagic Flux ◽  
Protective Effects ◽  
Renal Protection ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Proximal Tubular ◽  
Renal Proximal Tubular Cells ◽  
Renal Proximal Tubular

Obesity is supposed to cause renal injury via autophagy deficiency. Recently, sodium glucose co-transporter 2 inhibitors (SGLT2i) were reported to protect renal injury. However, the mechanisms of SGLT2i for renal protection are unclear. Here, we investigated the effect of SGLT2i for autophagy in renal proximal tubular cells (PTCs) on obesity mice. We fed C57BL/6J mice with a normal diet (ND) or high-fat and -sugar diet (HFSD) for nine weeks, then administered SGLT2i, empagliflozin, or control compound for one week. Each group contained N = 5. The urinary N-acetyl-beta-d-glucosaminidase level in the HFSD group significantly increased compared to ND group. The tubular damage was suppressed in the SGLT2i–HFSD group. In electron microscopic analysis, multi lamellar bodies that increased in autophagy deficiency were increased in PTCs in the HFSD group but significantly suppressed in the SGLT2i group. The autophagosomes of damaged mitochondria in PTCs in the HFSD group frequently appeared in the SGLT2i group. p62 accumulations in PTCs were significantly increased in HFSD group but significantly suppressed by SGLT2i. In addition, the mammalian target of rapamycin was activated in the HFSD group but significantly suppressed in SGLT2i group. These data suggest that SGLT2i has renal protective effects against obesity via improving autophagy flux impairment in PTCs on a HFSD.

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