Lindane affects phosphoiniositide turnover through a different mechanism of the phosphatidylinositol synthesis inhibition in rat renal proximal tubule cell culture

1994 ◽  
Vol 6 (4) ◽  
pp. 433-438 ◽  
Author(s):  
S. Senar ◽  
M.N. Recio ◽  
M.A. Pérez-Albarsanz
2015 ◽  
Vol 30 (1) ◽  
pp. 95-105 ◽  
Author(s):  
Lydia Aschauer ◽  
Giada Carta ◽  
Nadine Vogelsang ◽  
Eberhard Schlatter ◽  
Paul Jennings

2012 ◽  
Vol 303 (2) ◽  
pp. F266-F278 ◽  
Author(s):  
Šárka Lhoták ◽  
Sudesh Sood ◽  
Elise Brimble ◽  
Rachel E. Carlisle ◽  
Stephen M. Colgan ◽  
...  

Renal proximal tubule injury is induced by agents/conditions known to cause endoplasmic reticulum (ER) stress, including cyclosporine A (CsA), an immunosuppressant drug with nephrotoxic effects. However, the underlying mechanism by which ER stress contributes to proximal tubule cell injury is not well understood. In this study, we report lipid accumulation, sterol regulatory element-binding protein-2 (SREBP-2) expression, and ER stress in proximal tubules of kidneys from mice treated with the classic ER stressor tunicamycin (Tm) or in human renal biopsy specimens showing CsA-induced nephrotoxicity. Colocalization of ER stress markers [78-kDa glucose regulated protein (GRP78), CHOP] with SREBP-2 expression and lipid accumulation was prominent within the proximal tubule cells exposed to Tm or CsA. Prolonged ER stress resulted in increased apoptotic cell death of lipid-enriched proximal tubule cells with colocalization of GRP78, SREBP-2, and Ca2+-independent phospholipase A2 (iPLA2β), an SREBP-2 inducible gene with proapoptotic characteristics. In cultured HK-2 human proximal tubule cells, CsA- and Tm-induced ER stress caused lipid accumulation and SREBP-2 activation. Furthermore, overexpression of SREBP-2 or activation of endogenous SREBP-2 in HK-2 cells stimulated apoptosis. Inhibition of SREBP-2 activation with the site-1-serine protease inhibitor AEBSF prevented ER stress-induced lipid accumulation and apoptosis. Overexpression of the ER-resident chaperone GRP78 attenuated ER stress and inhibited CsA-induced SREBP-2 expression and lipid accumulation. In summary, our findings suggest that ER stress-induced SREBP-2 activation contributes to renal proximal tubule cell injury by dysregulating lipid homeostasis.


Physiology ◽  
1987 ◽  
Vol 2 (5) ◽  
pp. 160-164
Author(s):  
LP Karniski ◽  
PS Aronson

Recent experiments unexpectedly suggest that formate plays a critical role in chloride transport across cell membranes. In particular, active uptake of chloride in the renal proximal tubule cell occurs by chloride-formate exchange. Formate recycles from lumen to cell via nonionic diffusion of uncharged formic acid. In this manner, small amounts of formate can facilitate resorption of large quantities of chloride.


1985 ◽  
Vol 124 (3) ◽  
pp. 411-423 ◽  
Author(s):  
M. Anwar Waqar ◽  
Janny Seto ◽  
Soon Dong Chung ◽  
Sue Hiller-Grohol ◽  
Mary Taub

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