alexa Delivering Oxidation Resistance-1 (OXR1) to Mouse Kidney by Genetic Modified Mesenchymal Stem Cells Exhibited Enhanced Protection against Nephrotoxic Serum Induced Renal Injury and Lupus Nephritis
ISSN: 2157-7633

Journal of Stem Cell Research & Therapy
Open Access

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Research Article

Delivering Oxidation Resistance-1 (OXR1) to Mouse Kidney by Genetic Modified Mesenchymal Stem Cells Exhibited Enhanced Protection against Nephrotoxic Serum Induced Renal Injury and Lupus Nephritis

Yajuan Li2,5, Wei Li1, Chu Liu1, Mei Yan5, Indu Raman5, Yong Du3, Xiangdong Fang2, Xin J. Zhou4, Chandra Mohan3* and Quan-Zhen Li1,5*

1Key Laboratory of Medical Genetics, Wenzhou Medical University School of Laboratory Medicine & Life Science, Wenzhou, 325035, China

2Laboratory of Disease Genomics and Individualized Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, 100029, China

3Department of Biomedical Engineering, University of Houston, Houston, TX, 77204, USA

4Renal Path Diagnostics, Pathologist BioMedical Laboratories, Lewisville, TX, 75067, USA

5Department of Immunology and Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA

*Corresponding Authors:
Chandra Mohan
Department of Immunology and Internal Medicine
University of Texas Southwestern Medical Center
5323 Harry Hines Blvd. Dallas, Texas 75390-8814, USA
Tel: 2146456073
Fax: 2146456074
E-mail: [email protected]
 
Quan-Zhen Li
Department of Immunology and Internal Medicine
University of Texas Southwestern Medical Center
5323 Harry Hines Blvd. Dallas, Texas 75390-8814, USA
Tel: 2146456073
Fax: 2146456074
E-mail: [email protected]

Received date: August 25, 2014; Accepted date: September 08, 2014; Published date: September 10, 2014

Citation: Li Y, Li W, Liu C, Yan M, Raman I, et al. (2014) Delivering Oxidation Resistance-1 (OXR1) to Mouse Kidney by Genetic Modified Mesenchymal Stem Cells Exhibited Enhanced Protection against Nephrotoxic Serum Induced Renal Injury and Lupus Nephritis. J Stem Cell Res Ther 4: 231. doi: 10.4172/2157-7633.1000231

Copyright: © 2014 Li Y, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Objective: To elucidate the role of oxidation resistance 1 (OXR1) gene Oxidative stress plays a pivotal role in pathogenesis of immune-mediated nephritis. Recently we identified oxidation resistance 1 (OXR1) is conventionally expressed in eukaryotes and has an ability to prevent oxidative damage caused by various oxidative stresses. Although the protective effect of OXR1 in immune-associated inflammatory response and oxidative damage is not clear and will be investigated in this study. Methods: We utilized mesenchymal stem cells (MSCs) as vehicles to carry OXR1 into the injured kidneys of nephritis model mice and investigated the influence of OXR1 on glomerulonephritis. Human OXR1 gene was integrated into genome of MSCs via lentiviral vector, and established hOXR1-MSC cell line which still maintains the differentiation property. 129/svj mice with anti-glomerular basement membrane (GBM) challenge and spontaneous lupus mice B6.Sle1.Sle2.Sle3 were injected with hOXR1-MSCs (i.v. injection) to evaluate the function of hOXR1. Immunohistochemistry was used to appraise the renal pathology and Tunel staining was applied to detect cell apoptosis. Results: Compared with control mice, hOXR1-MSCs administration showed significantly decreased blood urea nitrogen (BUN), proteinuria and ameliorated renal pathological damage. And hOXR1-MSCs transplantation significantly reduced macrophage and T lymphocyte infiltration by inhibiting the expression of CCL2, CCL7, IL-1β, IL-6 and NFκB in mouse kidney. Moreover, hOXR1-MSCs prevented hydrogen peroxide (H2O2)-induced oxidative stress and its implantation reduced nitric oxide (NO) in mouse serum and urine to inhibit tubular cell apoptosis. Conclusion: OXR1-MSCs transplantation may exert a certain protective effect on nephritis by suppressing inflammation and oxidative stress.

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