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Associations between D3R expression in synovial mast cells and disease activity and oxidant status in patients with rheumatoid arthritis

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Abstract

Dopamine D3 receptor (D3R) on immune cells is involved in the pathogenesis of rheumatoid arthritis (RA). Mast cells (MCs) are currently identified as important effector cells in synovial inflammation of RA, but little is known about the role of D3R on synovial MCs in the pathogenesis of RA. Several inflammatory cells in the synovium induce reactive oxygen species (ROS) formation which are involved in the progression of RA. However, it is unclear whether D3R on synovial MCs is related to the levels of ROS in RA patients. In this study, a total of 73 patients with RA were divided into three groups according to disease activity DAS28 scores. The number of cases in group 1, group 2, and group 3 was 19, 26, and 28, respectively. We examined D3R-positive MC numbers in the synovial fluid and ROS levels in each group of RA patients, and we also analyzed the association of D3R-positive MC numbers with RA disease activity and ROS levels. MDA and protein carbonylation in the serum and synovial fluid were measured to reflect the level of lipid peroxidation and protein oxidation, respectively. Additionally, superoxide dismutase (SOD) and catalase (CAT) in the serum and synovial fluid were used to be markers of antioxidant levels. Our results showed that D3R-positive MCs in the synovial fluid showed a declining trend with the increased disease activity DAS28 score in RA patients. There was negative correlation between D3R-positive MC numbers in the synovial fluid and disease severity DAS28 score of RA patients. Moreover, D3R-positive MC numbers in the synovial fluid were negatively correlated with the level of MDA and protein carbonylation while were positively correlated with antioxidant levels such as SOD and CAT in RA patients. Our results suggested that D3R on MCs may be involved in ROS-mediated pathogenesis of RA.

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Funding

This study was supported by grants from the Shaanxi Province Natural Science Fund (2017JQ8032), the Fundamental Research Funds for the Central Universities of China (no. xjj2016109 to Xue Li), and the Key Project of the Second Affiliated Hospital of Xi’an Jiaotong University (YJ(ZD)201614 to Xue Li).

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Authors and Affiliations

  1. Department of Laboratory, The Second Affiliated Hospital of Medical College of Xi’an Jiaotong University, Xi’an, 710004, Shaanxi, People’s Republic of China

    Li Xue, Juntao He, Yanying Dong & Yan Geng

  2. Department of Rheumatology, The Second Affiliated Hospital of Medical College of Xi’an Jiaotong University, Xi’an, Shaanxi, China

    Xueyi Li

  3. The First Department of Rheumatology, Xi’an Fifth Hospital, Xi’an, Shaanxi, China

    Qingping Chen & Siyao Shen

  4. Department of Rheumatology, The First Affiliated Hospital of Medical College of Xi’an Jiaotong University, Xi’an, Shaanxi, China

    Jing Wang

  5. Department of Neurology, The First Affiliated Hospital of Medical College of Xi’an Jiaotong University, Xi’an, Shaanxi, China

    Rui Jia

  6. The Second Department of Orthopaedics, The Second Affiliated Hospital of Medical College of Xi’an Jiaotong University, Xi’an, Shaanxi, China

    Quan Jin Zang

  7. Department of Laboratory, Wuxi Maternity and Child Health Hospital, Nanjing Medical University, Wuxi, Jiangsu, China

    Ting Zhang

  8. Department of Cardiovascular Surgery, The First Affiliated Hospital of Medical College of Xi’an Jiaotong University, Xi’an, Shaanxi, China

    Ming Li

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  1. Li Xue
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Correspondence to Yan Geng.

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All procedures performed in this study involving human participants were in accordance with the ethical standards of the Research Committee of Human Investigation of Medical College of Xi’an Jiaotong University. All participants gave informed consent.

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Xue, L., Li, X., Chen, Q. et al. Associations between D3R expression in synovial mast cells and disease activity and oxidant status in patients with rheumatoid arthritis. Clin Rheumatol 37, 2621–2632 (2018). https://doi.org/10.1007/s10067-018-4168-1

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