The rheumatoid arthritis shared epitope increases cellular susceptibility to oxidative stress by antagonizing an adenosine-mediated anti-oxidative pathway

The rheumatoid arthritis shared epitope increases cellular susceptibility to oxidative stress by antagonizing an adenosine-mediated anti-oxidative pathway Song Ling1, Zhanguo Li1,2, Olga Borschukova3, Liqun Xiao1, Paul Pumpens3 and Joseph Holoshitz1 1Department 2Department of Internal Medicine, University of Michigan, 1150 W. Medical Center Dr., 5520 MSRB I, Ann Arbor, MI 48109-0680, USA of Rheumatology, Beijing Medical University, Beijing, 11 S. Xizhimen Blvd, Beijing, 100044, The People's Republic of China 3Biomedical Research and Study Center, University of Latvia, Ratsupites 1, Riga, LV-1067, Latvia Corresponding author: Joseph Holoshitz, jholo@ Received: 19 Oct 2006 Revisions requested: 24 Nov 2006 Revisions received: 17 Dec 2006 Accepted: 25 Jan. | Available online http content 9 1 R5 Open Access Research article The rheumatoid arthritis shared epitope increases cellular susceptibility to oxidative stress by antagonizing an adenosine-mediated anti-oxidative pathway Song Ling1 Zhanguo Li1 2 Olga Borschukova3 Liqun Xiao1 Paul Pumpens3 and Joseph Holoshitz1 Department of Internal Medicine University of Michigan 1150 W. Medical Center Dr. 5520 MSRB I Ann Arbor MI 48109-0680 USA department of Rheumatology Beijing Medical University Beijing 11 S. Xizhimen Blvd Beijing 100044 The People s Republic of China 3Biomedical Research and Study Center University of Latvia Ratsupites 1 Riga LV-1 067 Latvia Corresponding author Joseph Holoshitz jholo@ Received 19 Oct 2006 Revisions requested 24 Nov 2006 Revisions received 1 7 Dec 2006 Accepted 25 Jan 2007 Published 25 Jan 2007 Arthritis Research Therapy 2007 9 R5 doi ar2111 This article is online at http content 9 1 R5 2007 Ling et al. licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract We have recently demonstrated that the rheumatoid arthritis RA shared epitope SE acts as a ligand that triggers nitric oxide NO signaling in opposite cells. Given the known prooxidative effect of NO and the proposed role of oxidative stress in the pathogenesis of RA this study explores whether SE-triggered signaling can increase cellular oxidative stress. cAMP levels adenylyl cyclase activity and protein kinase A activity were measured using commercial kits. Generation of reactive oxygen species ROS was quantified using the fluorochrome dichlorofluorescein diacetate. Oxidative DNA damage was quantified using the single-cell electrophoresis technique. Here we report that cells exposed .

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