Glutathione S-transferase Mu 2-transduced mesenchymal stem cells ameliorated anti-glomerular basement membrane antibody-induced glomerulonephritis by inhibiting oxidation and inflammation

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• 作者：Yajuan Li (1) (2)
  Mei Yan (1)
  Jichen Yang (3)
  Indu Raman (1)
  Yong Du (4)
  Soyoun Min (1)
  Xiangdong Fang (2)
  Chandra Mohan (1) (4)
  Quan-Zhen Li (1) (5)
  
• 刊名：Stem Cell Research & Therapy
• 出版年：2014
• 出版时间：March 2014
• 年：2014
• 卷：5
• 期：1
• 全文大小：961 KB
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• 作者单位：Yajuan Li (1) (2)
  Mei Yan (1)
  Jichen Yang (3)
  Indu Raman (1)
  Yong Du (4)
  Soyoun Min (1)
  Xiangdong Fang (2)
  Chandra Mohan (1) (4)
  Quan-Zhen Li (1) (5)
  
  1. Department of Immunology and Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX, 75390-8814, USA
  2. Laboratory of Disease Genomics and Individualized Medicine, Key Laboratory of Genome Sciences and Information, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, 100101, China
  3. Division of Biostatistics, Department of Clinical Sciences, University of Texas Southwestern Medical Center at Dallas, Dallas, TX, 75390, USA
  4. Biomedical Engineering Department, University of Houston, Houston, TX, 77204, USA
  5. Key Laboratory of Medical Genetics, Wenzhou Medical University School of Laboratory Medicine and Life Science, Wenzhou, 325035, China
  
• ISSN：1757-6512

文摘

Introduction Oxidative stress is implicated in tissue inflammation, and plays an important role in the pathogenesis of immune-mediated nephritis. Using the anti-glomerular basement membrane antibody-induced glomerulonephritis (anti-GBM-GN) mouse model, we found that increased expression of glutathione S-transferase Mu 2 (GSTM2) was related to reduced renal damage caused by anti-GBM antibodies. Furthermore, mesenchymal stem cell (MSC)-based therapy has shed light on the treatment of immune-mediated kidney diseases. The aim of this study was to investigate if MSCs could be utilized as vehicles to deliver the GSTM2 gene product into the kidney and to evaluate its potential therapeutic effect on anti-GBM-GN. Methods The human GSTM2 gene (hGSTM2) was transduced into mouse bone marrow-derived MSCs via a lentivirus vector to create a stable cell line (hGSTM2-MSC). The cultured hGSTM2-MSCs were treated with 0.5mM H2O2, and apoptotic cells were measured by terminal dUTP nick-end labeling (TUNEL) assay. The 129/svj mice, which were challenged with anti-GBM antibodies, were injected with 106 hGSTM2-MSCs via the tail vein. Expression of hGSTM2 and inflammatory cytokines in the kidney was assayed by quantitative PCR and western blotting. Renal function of mice was evaluated by monitoring proteinuria and levels of blood urea nitrogen (BUN), and renal pathological changes were analyzed by histochemistry. Immunohistochemical analysis was performed to measure inflammatory cell infiltration and renal cell apoptosis. Results MSCs transduced with hGSTM2 exhibited similar growth and differentiation properties to MSCs. hGSTM2-MSCs persistently expressed hGSTM2 and resisted H2O2-induced apoptosis. Upon injection into 129/svj mice, hGSTM2-MSCs migrated to the kidney and expressed hGSTM2. The anti-GBM-GN mice treated with hGSTM2-MSCs exhibited reduced proteinuria and BUN (58% and 59% reduction, respectively) and ameliorated renal pathological damage, compared with control mice. Mice injected with hGSTM2-MSCs showed alleviated renal inflammatory cell infiltration and reduced expression of chemokine (C-C motif) ligand 2 (CCL2), interleukin (IL)-1β and IL-6 (53%, 46% and 52% reduction, respectively), compared with controls. Moreover, hGSTM2-MSCs increased expression of renal superoxide dismutase and catalase, which may associate with detoxifying reactive oxygen species to prevent oxidative renal damage. Conclusions Our data suggest that the enhanced protective effect of GSTM2-transduced MSCs against anti-GBM-GN might be associated with inhibition of oxidative stress-induced renal cell apoptosis and inflammation, through over-expression of hGSTM2 in mouse kidneys.