| 논문분류 | |
|---|---|
| 제목 | C/EBP Homologous Protein (CHOP)-gene Deletion Attenuates Kidney Ischemia/Reperfusion Injury in Mice |
| 저자 | Mi Ra Noh1, Jee In Kim2, Kwon Moo Park1 |
| 출판정보 | 2014; 2014(1): |
| 키워드 | ER stress, CHOP, Ischemia |
| 초록 | Endoplasmic reticulum (ER) has been implicated in the pathology of renal ischemia/reperfusion (I/R). C/EBP homologous protein (CHOP) is an important mediator of ER stress-induced cell and organ injury. Here, we investigated the role of CHOP in I/R-induced kidney injury using CHOP-knockout (CHOP-/-) and their wild-type (CHOP+/+) mice. Mice were subjected to either 30 minutes of bilateral renal ischemia or sham-operation as a control. Twenty-four hours after ischemia, concentrations of plasma creatinine (PCr) and blood urea nitrogen (BUN) were significantly increased in both mice. The increases of PCr and BUN concentrations were less in CHOP-/- than in CHOP+/+ mice. 24 hours after ischemia, tubules disrupted and congested appeared in the outer medulla in the periodic acid Schiff (PAS)-stained kidney sections of both CHOP-/- and CHOP+/+ mice. The damage scores of kidneys after ischemia were lower in CHOP-/- mice than CHOP+/+ mice. When the cleavage of PARP and activation of caspase 3 in the kidney lysates were evaluated by western blotting, the cleavage of PARP and activation of caspase 3 were less in CHOP-/- mice than in CHOP+/+ mice. These results indicate that CHOP-deficiency attenuates susceptibility to kidney injury by inhibition of necrosis and apoptosis in tubular epithelial cells, suggesting CHOP is a potential therapeutic target protein in I/R injury. |
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