scholarly journals Membrane raft redox signalling contributes to renal tubular cell epithelial–mesenchymal transition and fibrosis and inflammation of the kidneys

2018 ◽  
Vol 596 (18) ◽  
pp. 4297-4298
Author(s):  
Haisam Shah ◽  
Alison Hacker
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Tubular Cell ◽  
Renal Tubular Cell ◽  
Membrane Raft ◽  
Mesenchymal Transition ◽  
Redox Signalling ◽  
Renal Tubular

scholarly journals MicroRNA-328 Inhibits Renal Tubular Cell Epithelial-to-Mesenchymal Transition by Targeting the CD44 in Pressure-Induced Renal Fibrosis

PLoS ONE ◽  
2014 ◽  
Vol 9 (6) ◽  
pp. e99802 ◽  
Author(s):  
Cheng-Hsien Chen ◽  
Chung-Yi Cheng ◽  
Yen-Cheng Chen ◽  
Yuh-Mou Sue ◽  
Chung-Te Liu ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Epithelial To Mesenchymal Transition ◽  
Tubular Cell ◽  
Renal Tubular Cell ◽  
Mesenchymal Transition ◽  
Renal Tubular

scholarly journals AT1 and AT2 receptors modulate renal tubular cell necroptosis in angiotensin II-infused renal injury mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Yongjun Zhu ◽  
Hongwang Cui ◽  
Jie Lv ◽  
Haiqin Liang ◽  
Yanping Zheng ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Renal Injury ◽  
Critical Role ◽  
Kidney Injury ◽  
Renin Angiotensin System ◽  
Tubular Cell ◽  
Tubular Damage ◽  
Renal Tubular Cell ◽  
Ang Ii ◽  
Renal Tubular

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.

scholarly journals TO012GADD45G PREVENTS ACUTE RENAL TUBULAR CELL NECROSIS

2016 ◽  
Vol 31 (suppl_1) ◽  
pp. i65-i65
Author(s):  
Gyu-Tae Shin ◽  
Hwa-Jung Lee ◽  
Heungsoo Kim
Keyword(s):  
Tubular Cell ◽  
Renal Tubular Cell ◽  
Cell Necrosis ◽  
Renal Tubular

Propylene glycol-induced proximal renal tubular cell injury

1997 ◽  
Vol 30 (1) ◽  
pp. 134-139 ◽  
Author(s):  
Peter D. Yorgin ◽  
Andreas A. Theodorou ◽  
Amira Al-Uzri ◽  
Karen Davenport ◽  
Leslie V. Boyer-Hassen ◽  
...  
Keyword(s):  
Propylene Glycol ◽  
Cell Injury ◽  
Tubular Cell ◽  
Renal Tubular Cell ◽  
Renal Tubular
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