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논문분류	춘계학술대회 초록집
제목	TonEBP transcription factor mediates oxidative damages in the kidney in response to ischemia-reperfusion
저자	Eunjin Yoo1, Mijin Kwon1, Sunwoo Lim2, Sora Yoon1, Dougu Nam1, Sooyoun Choi1, Whaseon Lee1, Hyugmoo Kwon1
출판정보	2018; 2018(1):
키워드	TonEBP \| NFAT5 \| AKI \| Ischemia-Reperfusion
초록	Objectives: TonEBP transcription factor is a key regulator of inflammatory diseases such as rheumatoid arthritis and atherosclerosis. Since inflammation is involved in the pathophysiology of acute renal failure resulting from ischemia, we aimed to identify the role of TonEBP in ischemia-reperfusion (IR). Methods: We examined the role of TonEBP using a line of TonEBP haplo-deficient mice after 30 min of bilateral renal ischemia followed by reperfusion for 24 h. Renal epithelial cell line (HK-2) was used for in vitro experiments in response to hypoxia, ATP depletion, and hydrogen peroxide with siRNA-mediated knockdown of TonEBP. Results: In the TonEBP haplo-deficient animals, induction of TonEBP expression, oxidative stress, inflammation, cell death, and functional injury in the kidney in response to IR were all reduced. Renal transcriptome analysis revealed that genes in several pathways such as peroxisome and mitochondrial inner membrane were suppressed in response to IR, and the suppression was relieved in the TonEBP deficient animals. Cellular injury and oxidative stress were reproduced in a renal epithelial cell line in response to hypoxia, ATP depletion, or hydrogen peroxide. Knockdown of TonEBP reduced the injury and intracellular reactive oxygen species in correlation with increased expression of the suppressed genes in the kidney after IR. Conclusions: These results indicate that TonEBP mediates oxidative damages in the kidney by suppressing genes involved in cellular metabolism. Hence, TonEBP may potentially be a critical target for prevention of acute kidney injury.
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