Uric acid and angiotensin II additively promote inflammation and oxidative stress in human proximal tubule cells by activation of toll‐like receptor 4

2018 ◽  
Vol 234 (7) ◽  
pp. 10868-10876 ◽  
Author(s):  
Samantha Milanesi ◽  
Daniela Verzola ◽  
Francesca Cappadona ◽  
Barbara Bonino ◽  
Abitha Murugavel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Angiotensin Ii ◽  
Proximal Tubule ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Proximal Tubule Cells ◽  
Tubule Cells ◽  
And Oxidative Stress ◽  
Human Proximal Tubule

scholarly journals Uric Acid Promotes Apoptosis in Human Proximal Tubule Cells by Oxidative Stress and the Activation of NADPH Oxidase NOX 4

PLoS ONE ◽  
2014 ◽  
Vol 9 (12) ◽  
pp. e115210 ◽  
Author(s):  
Daniela Verzola ◽  
Elena Ratto ◽  
Barbara Villaggio ◽  
Emanuele Luigi Parodi ◽  
Roberto Pontremoli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Nadph Oxidase ◽  
Proximal Tubule ◽  
Proximal Tubule Cells ◽  
Tubule Cells ◽  
Human Proximal Tubule

scholarly journals Electrophysiology and ultrastructure of cultured human proximal tubule cells

1988 ◽  
Vol 33 (2) ◽  
pp. 508-516 ◽  
Author(s):  
John G. Blackburn ◽  
Debra J. Hazen-Martin ◽  
Carol J. Detrisac ◽  
Donald A. Sens
Keyword(s):  
Proximal Tubule ◽  
Proximal Tubule Cells ◽  
Tubule Cells ◽  
Human Proximal Tubule

scholarly journals Uremic Toxins Induce ET-1 Release by Human Proximal Tubule Cells, which Regulates Organic Cation Uptake Time-Dependently

Cells ◽  
2015 ◽  
Vol 4 (3) ◽  
pp. 234-252 ◽  
Author(s):  
Carolien Schophuizen ◽  
Joost Hoenderop ◽  
Rosalinde Masereeuw ◽  
Lambert Heuvel
Keyword(s):  
Proximal Tubule ◽  
Organic Cation ◽  
Uremic Toxins ◽  
Proximal Tubule Cells ◽  
Cation Uptake ◽  
Tubule Cells ◽  
Human Proximal Tubule

Toxicoproteomic Analysis of Poly(ADP-Ribose)-Associated Proteins Induced by Oxidative Stress in Human Proximal Tubule Cells

2019 ◽  
Vol 171 (1) ◽  
pp. 117-131
Author(s):  
Argel Islas-Robles ◽  
Deepthi Yedlapudi ◽  
Serrine S Lau ◽  
Terrence J Monks
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Proximal Tubule ◽  
Calcium Influx ◽  
Regulation Of Transcription ◽  
Loss Of Function ◽  
Proximal Tubule Cells ◽  
Associated Proteins ◽  
Tubule Cells ◽  
Parp 1

Abstract 2,3,5-Tris-(glutathion-S-yl)hydroquinone (TGHQ) is a nephrotoxic and nephrocarcinogenic metabolite of hydroquinone. TGHQ generates reactive oxygen species (ROS), causing DNA-strand breaks, hyperactivation of PARP-1, increases in intracellular calcium ([Ca2+]i), and cell death. PARP-1 catalyzes the attachment of ADP-ribose polymers (PAR) to target proteins. In human kidney proximal tubule cells, ROS-mediated PARP-1 hyperactivation and elevations in [Ca2+]i are reciprocally coupled. The molecular mechanism of this interaction is unclear. The aim of the present study was to identify ROS-induced PAR-associated proteins to further understand their potential role in cell death. PAR-associated proteins were enriched by immunoprecipitation, identified by LC-MS/MS, and relative abundance was obtained by spectral counting. A total of 356 proteins were PAR-modified following TGHQ treatment. A total of 13 proteins exhibited gene ontology annotations related to calcium. Among these proteins, the general transcription factor II-I (TFII-I) is directly involved in the modulation of [Ca2+]i. TFII-I binding to phospholipase C (PLC) leads to calcium influx via the TRPC3 channel. However, inhibition of TRPC3 or PLC had no effect on TGHQ-mediated cell death, suggesting that their loss of function may be necessary but insufficient to cause cell death. Nevertheless, TGHQ promoted a time-dependent translocation of TFII-I from the nucleus to the cytosol concomitant with a decrease in tyrosine phosphorylation in α/β-TFII-I. Therefore it is likely that ROS have an important impact on the function of TFII-I, such as regulation of transcription, and DNA translesion synthesis. Our data also shed light on PAR-mediated signaling during oxidative stress, and contributes to the development of strategies to prevent PAR-dependent cell death.

Sign in / Sign up

Export Citation Format

Share Document