Selective fatty acid release from intracellular phospholipids caused by PCBs in rat renal tubular cell cultures

2000 ◽  
Vol 125 (2) ◽  
pp. 117-131 ◽  
Author(s):  
E Sánchez ◽  
M Fernández Santiago ◽  
P López-Aparicio ◽  
M.N Recio ◽  
M.A Pérez-Albarsanz
2001 ◽  
Vol 13 (2) ◽  
pp. 111-118 ◽  
Author(s):  
Mercedes Fernández Santiago ◽  
Pilar López-Aparicio ◽  
Marı́a N. Recio ◽  
Miguel A. Pérez-Albarsanz

1997 ◽  
Vol 57 (1) ◽  
pp. 54-62 ◽  
Author(s):  
P. López-Aparicio ◽  
M.J. Merino ◽  
E. Sánchez ◽  
M.N. Recio ◽  
M.A. Pérez-Albarsanz

1994 ◽  
Vol 83 (02) ◽  
pp. 85-86
Author(s):  
A. Delbancut ◽  
M.A. Barrouillet ◽  
R. Maury-Brachet ◽  
A. Boudou ◽  
P. Dorfman ◽  
...  

2006 ◽  
Vol 163 (2) ◽  
pp. 91-100 ◽  
Author(s):  
Mercedes Fernández Santiago ◽  
Pedro L. Pérez-Reyes ◽  
Pilar López-Aparicio ◽  
María N. Recio ◽  
Miguel A. Pérez-Albarsanz

2007 ◽  
Vol 21 (2) ◽  
pp. 68-75
Author(s):  
Mercedes Fernández Santiago ◽  
Pilar López-Aparicio ◽  
María N. Recio ◽  
Miguel A. Pérez-Albarsanz

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Yongjun Zhu ◽  
Hongwang Cui ◽  
Jie Lv ◽  
Haiqin Liang ◽  
Yanping Zheng ◽  
...  

AbstractAbnormal renin-angiotensin system (RAS) activation plays a critical role in the initiation and progression of chronic kidney disease (CKD) by directly mediating renal tubular cell apoptosis. Our previous study showed that necroptosis may play a more important role than apoptosis in mediating renal tubular cell loss in chronic renal injury rats, but the mechanism involved remains unknown. Here, we investigate whether blocking the angiotensin II type 1 receptor (AT1R) and/or angiotensin II type 2 receptor (AT2R) beneficially alleviates renal tubular cell necroptosis and chronic kidney injury. In an angiotensin II (Ang II)-induced renal injury mouse model, we found that blocking AT1R and AT2R effectively mitigates Ang II-induced increases in necroptotic tubular epithelial cell percentages, necroptosis-related RIP3 and MLKL protein expression, serum creatinine and blood urea nitrogen levels, and tubular damage scores. Furthermore, inhibition of AT1R and AT2R diminishes Ang II-induced necroptosis in HK-2 cells and the AT2 agonist CGP42112A increases the percentage of necroptotic HK-2 cells. In addition, the current study also demonstrates that Losartan and PD123319 effectively mitigated the Ang II-induced increases in Fas and FasL signaling molecule expression. Importantly, disruption of FasL significantly suppressed Ang II-induced increases in necroptotic HK-2 cell percentages, and necroptosis-related proteins. These results suggest that Fas and FasL, as subsequent signaling molecules of AT1R and AT2R, might involve in Ang II-induced necroptosis. Taken together, our results suggest that Ang II-induced necroptosis of renal tubular cell might be involved both AT1R and AT2R and the subsequent expression of Fas, FasL signaling. Thus, AT1R and AT2R might function as critical mediators.


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