Intraarticular gene transfer of SPRY2 suppresses adjuvant-induced arthritis in rats

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• 作者：Wei Zhang ; Jingying Zhu ; Zhiyan Du ; Jiyun Yu…
• 关键词：SPRY2 ; Rheumatoid arthritis ; Gene therapy ; Inflammatory signals ; Inflammatory mediators
• 刊名：Applied Microbiology and Biotechnology
• 出版年：2015
• 出版时间：August 2015
• 年：2015
• 卷：99
• 期：16
• 页码：6727-6735
• 全文大小：3,539 KB
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• 作者单位：Wei Zhang (1)
  Jingying Zhu (1)
  Zhiyan Du (1)
  Jiyun Yu (1)
  Yuanji Xu (1)
  Fang Wang (1)
  
  1. Department of Translational Medicine, Beijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, 100850, China
  
• 刊物类别：Chemistry and Materials Science
• 刊物主题：Chemistry
  Biotechnology
  Microbiology
  Microbial Genetics and Genomics
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：1432-0614

文摘

AKT and ERK pathways have been implicated as therapeutic targets for human rheumatoid arthritis (RA), fibroblast-like synoviocytes (FLS) inhibition, and thus RA treatment. Sprouty2 (SPRY2) has been known as a tumor suppressor by blocking both ERK and AKT signaling cascades. Whether SPRY2 can function as a suppressor of tumor-like inflammatory FLS and RA through negatively regulating AKT and ERK activation has not been reported. The purpose of this study was to determine whether SPRY2 might have antiarthritic effects in experimental animal model of RA. We first determined that expression of SPRY2 mRNA was decreased in FLS from patients with RA compared with patients with osteoarthritis (OA). Further studies demonstrated that intraarticular gene transfer with AdSPRY2, the recombinant adenovirus containing SPRY2 complementary DNA, resulted in a significant suppression of rat adjuvant-induced arthritis (AIA) compared with the control AdGFP, the adenoviral vector encoding green fluorescent protein, as reflected in both clinical and histological observations. AdSPRY2 suppressed the production of proinflammatory cytokines and matrix metalloproteinases (MMPs), and the activation of ERK and AKT signals in AIA ankle joints. These results suggest that using SPRY2 to block the AKT and ERK pathways effectively reduces the inflammatory responses and arthritic progression in AIA. Thus, the development of an immunoregulatory strategy based on SPRY2 may therefore have therapeutic potential in the treatment of RA.