Carbon Monoxide Inhibits the Nuclear-cytoplasmic Translocation of HMGB1 in an In Vitro Oxidative Stress Injury Model of Mouse Renal Tubular Epithelial Cells
单位：[1]Institute of Organ Transplantation, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China华中科技大学同济医学院附属同济医院器官移植研究所器官移植[2]Key Laboratory of Organ Transplantation, Ministry of Education; Key Laboratory of Organ Transplantation, Ministry of Health, Wuhan 430030, China
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.
基金：
National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81300574]
第一作者单位：[1]Institute of Organ Transplantation, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China[2]Key Laboratory of Organ Transplantation, Ministry of Education; Key Laboratory of Organ Transplantation, Ministry of Health, Wuhan 430030, China
通讯作者：
通讯机构：[1]Institute of Organ Transplantation, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China[2]Key Laboratory of Organ Transplantation, Ministry of Education; Key Laboratory of Organ Transplantation, Ministry of Health, Wuhan 430030, China
推荐引用方式(GB/T 7714)：
jia yu,wang lu,zhao guang-yuan,et al.Carbon Monoxide Inhibits the Nuclear-cytoplasmic Translocation of HMGB1 in an In Vitro Oxidative Stress Injury Model of Mouse Renal Tubular Epithelial Cells[J].JOURNAL OF HUAZHONG UNIVERSITY OF SCIENCE AND TECHNOLOGY-MEDICAL SCIENCES.2016,36(6):791-795.doi:10.1007/s11596-016-1663-y.
APA：
jia,yu,wang,lu,zhao,guang-yuan,wang,zhi-qiang,chen,song&chen,gang.(2016).Carbon Monoxide Inhibits the Nuclear-cytoplasmic Translocation of HMGB1 in an In Vitro Oxidative Stress Injury Model of Mouse Renal Tubular Epithelial Cells.JOURNAL OF HUAZHONG UNIVERSITY OF SCIENCE AND TECHNOLOGY-MEDICAL SCIENCES,36,(6)
MLA：
jia,yu,et al."Carbon Monoxide Inhibits the Nuclear-cytoplasmic Translocation of HMGB1 in an In Vitro Oxidative Stress Injury Model of Mouse Renal Tubular Epithelial Cells".JOURNAL OF HUAZHONG UNIVERSITY OF SCIENCE AND TECHNOLOGY-MEDICAL SCIENCES 36..6(2016):791-795
