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Author

Kwon, H. Moo
Inflammation and Kidney Disorder Lab
Research Interests
  • TonEBP, Obesity, Cancer, Chronic inflammatory diseases, Brain disorder, Kidney disorders, Genomic instability

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Multiple cell death pathways are independently activated by lethal hypertonicity in renal epithelial cells

Cited 1 times inthomson ciCited 2 times inthomson ci
Title
Multiple cell death pathways are independently activated by lethal hypertonicity in renal epithelial cells
Author
Choi, Soo YounLee-Kwon, WhaseonLee, Hwan HeeLee, Jun HoSanada, SatoruKwon, H. Moo
Keywords
Caspase; Cathepsin B; Cytochrome c
Issue Date
201311
Publisher
AMER PHYSIOLOGICAL SOC
Citation
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, v.305, no.10, pp.C1011 - C1020
Abstract
When hypertonicity is imposed with sufficient intensity and acuteness, cells die. Here we investigated the cellular pathways involved in death using a cell line derived from renal epithelium. We found that hypertonicity rapidly induced activation of an intrinsic cell death pathway- release of cytochrome c and activation of caspase-3 and caspase-9-and an extrinsic pathway-activation of caspase-8. Likewise, a lysosomal pathway of cell death characterized by partial lysosomal rupture and release of cathepsin B from lysosomes to the cytosol was also activated. Relationships among the pathways were examined using specific inhibitors. Caspase inhibitors did not affect cathepsin B release into the cytosol by hypertonicity. In addition, cathepsin B inhibitors and caspase inhibitors did not affect hyper-tonicity-induced cytochrome c release, suggesting that the three pathways were independently activated. Combined inhibition of caspases and cathepsin B conferred significantly more protection from hypertonicity-induced cell death than inhibition of caspase or cathepsin B alone, indicating that all the three pathways contributed to the hypertonicity-induced cell death. Similar pattern of sensitivity to the inhibitors was observed in two other cell lines derived from renal epithelia. We conclude that multiple cell death pathways are independently activated early in response to lethal hypertonic stress in renal epithelial cells.
URI
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DOI
http://dx.doi.org/10.1152/ajpcell.00384.2012
ISSN
0363-6143
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