Journal
FREE RADICAL RESEARCH
Volume 45, Issue 6, Pages 692-698Publisher
TAYLOR & FRANCIS LTD
DOI: 10.3109/10715762.2011.567985
Keywords
Extracellular-superoxide dismutase; endoplasmic reticulum stress; thapsigargin; chronic kidney disease; extracellular-signal regulated kinase
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Funding
- Japan Society for the Promotion for Science [21790153, 21590169]
- Grants-in-Aid for Scientific Research [21590169, 21790153] Funding Source: KAKEN
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It has been reported that tubular cells suffer an endoplasmic reticulum (ER) stress during the development of chronic kidney disease, which is a potent risk factor of cardiovascular disease. Moreover, under these conditions, reactive oxygen species are generated and induce cell injury. Extracellular-superoxide dismutase (EC-SOD) is a member of SODs and protects the cells from oxidative stress. Here, it is demonstrated that thapsigargin, an ER stress inducer, decreased EC-SOD expression, whereas the expression of Cu, Zn-SOD and Mn-SOD was not changed. On the other hand, another ER stress inducer, tunicamycin, did not affect the expression of EC-SOD. Further, it was shown that thapsigargin has the ability to activate extracellular-signal regulated kinase (ERK), but tunicamycin does not. Moreover, pre-treatment with U0126, an inhibitor of mitogen-activated protein kinase kinase (MEK)/ERK, suppressed thapsigargin-triggered EC-SOD reduction, suggesting that MEK/ERK signalling should play an important role in the regulation of EC-SOD in COS7 cells under ER stress conditions.
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