Carbon monoxide inhibits the nuclear-cytoplasmic translocation of HMGB1 in an in vitro oxidative stress injury model of mouse renal tubular epithelial cells

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• 作者：Yu Jia 贾 钰 ; Lu Wang 王 璐 ; Guang-yuan Zhao 赵光远…
• 关键词：renal tubules ; epithelial cell ; oxidative stress ; HMGB1 protein ; carbon monoxide ; acetylation
• 刊名：Journal of Huazhong University of Science and Technology [Medical Sciences]
• 出版年：2016
• 出版时间：December 2016
• 年：2016
• 卷：36
• 期：6
• 页码：791-795
• 全文大小：
• 刊物主题：Medicine/Public Health, general;
• 出版者：Huazhong University of Science and Technology
• ISSN：1993-1352
• 卷排序：36

文摘

Carbon monoxide (CO), as a vital small molecule in signaling pathways, is found to be involved in ischemia-reperfusion injury (IRI) in renal transplantation. CO-releasing molecule-2 (CORM-2), a CO-releasing molecule, is a type of metal carbonyl complexes which can quickly release CO in vivo. In this study, an in vitro oxidative stress injury model was established to examine the effect of CORM-2 pretreatment on the nuclear-cytoplasmic translocation of high mobility group box 1 protein (HMGB1) in mouse primary renal proximal tubular epithelial cells (RPTECs). Immunofluorescence staining showed that HMGB1 in the medium- and CORM-2-treated groups was predominantly localized in the nucleus of the cells, whereas higher amounts of HMGB1 translocated to the cytoplasm in the H₂O₂- and inactive CORM-2 (iCORM-2)-treated groups. Western blotting of HMGB1 showed that the total amounts of cytoplasmic HMGB1 in the H₂O₂-treated (0.59±0.27) and iCORM-2-treated (0.57±0.22) groups were markedly higher than those in the medium-treated (0.19±0.05) and CORM-2-treated (0.21±0.10) groups (P<0.05). Co-immunoprecipitation showed that the levels of acetylated HMGB1 in the H₂O₂-treated (642.98±57.25) and iCORM-2-treated (342.11±131.25) groups were markedly increased as compared with the medium-treated (78.72±74.17) and CORM-2-treated (71.42±53.35) groups (P<0.05), and no significant difference was observed between the medium-treated and CORM-2-treated groups (P>0.05). In conclusion, our study demonstrated that in the in vitro oxidative stress injury model of primary RPTECs, CORM-2 can significantly inhibit the nuclear-cytoplasmic translocation of HMGB1, which is probably associated with the prevention of HMGB1 acetylation.