Angiotensin II triggers RIPK3-MLKL-mediated necroptosis by activating the Fas/FasL signaling pathway in renal tubular cells

PloS One
Yongjun ZhuLiangbao Zhong

Abstract

Our earlier studies proved that RIPK3-mediated necroptosis might be an important mode of renal tubular cell death in rats with chronic renal injury and the necroptotic cell death can be triggered by tumor necrosis factor-α (TNF-α) in vitro, but the triggering role of angiotensin II (AngII), which exerts notable effects on renal cells for the initiation and progression of renal tubulointerstitial fibrosis, is largely unknown. Here, we identified the presence of necroptotic cell death in the tubular cells of AngII-induced chronic renal injury and fibrosis mice and assessed the percentage of necroptotic renal tubular cell death with the disruption of this necroptosis by the addition of necrostatin-1 (Nec-1). Furthermore, the observation was further confirmed in HK-2 cells treated with AngII and RIPK1/3 or MLKL inhibitors. The detection of Fas and FasL proteins led us to investigate the contribution of the Fas/FasL signaling pathway to AngII-induced necroptosis. Disruption of FasL decreased the percentage of necroptotic cells, suggesting that Fas and FasL are likely key signal molecules in the necroptosis of HK-2 cells induced by AngII. Our data suggest that AngII exposure might trigger RIPK3-MLKL-mediated necroptosis in renal tubu...Continue Reading

References

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Citations

Sep 19, 2020·Infectious Diseases·Leonardo LorenteAlejandro Jiménez
Apr 3, 2021·Molecular and Cellular Endocrinology·Elena Cantero-NavarroAlberto Ortiz
Oct 8, 2020·Journal of Lipid and Atherosclerosis·Makoto Taniguchi, Toshiro Okazaki

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Methods Mentioned

BETA
transfection
Protein Assay
electrophoresis
confocal microscopy
transmission electron microscopy
RIP
flow cytometry

Software Mentioned

Image Lab
SPSS

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