Analysis of candidate genes of spontaneous arthritis in mice deficient for interleukin-1 receptor antagonist

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  • Cao Yanhong
    Institute of Kaschin-Beck Disease, Center for Endemic Disease Control, Centers for Disease Control and Prevention, Harbin Medical University Departments of Orthopaedic Surgery-Campbell Clinic, and Pathology, University of Tennessee Health Science Center (UTHSC)
  • Li Caijuan
    Department of Ultrasound, Hongqi Hospital of Mudanjiang Medical University
  • Yan Jian
    Department of Medicine, University of Tennessee Health Science Center
  • Jiao Feng
    Departments of Orthopaedic Surgery-Campbell Clinic, and Pathology, University of Tennessee Health Science Center (UTHSC)
  • Liu XiaoYun
    Departments of Orthopaedic Surgery-Campbell Clinic, and Pathology, University of Tennessee Health Science Center (UTHSC)
  • Hasty Karen A.
    Departments of Orthopaedic Surgery-Campbell Clinic, and Pathology, University of Tennessee Health Science Center (UTHSC)
  • Stuart John M.
    Department of Medicine, University of Tennessee Health Science Center
  • Gu Weikuan
    Departments of Orthopaedic Surgery-Campbell Clinic, and Pathology, University of Tennessee Health Science Center (UTHSC)
  • Jiao Yan
    Departments of Orthopaedic Surgery-Campbell Clinic, and Pathology, University of Tennessee Health Science Center (UTHSC)

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Previously, we identified a major quantitative trait locus (QTL) on mouse chromosome 1 that regulates the susceptibility to arthritis in an F2 population generated from arthritis-prone BALB/c and arthritis-resistant DBA/1 mice deficient for interleukin-1 receptor antagonist. To further select candidate genes for the QTL, we analyzed the expression patterns of arthritis in 38 F2 individuals and compared the expression levels of key candidate genes to the parental strains. Two distinct subpopulations of arthritic mice were identified in the 38 F2 mice. One subgroup of diseased mice was characterized by myeloid cell dominant inflammation, whereas the other was mainly associated with increased anti-apoptotic activities of inflammatory cells. Several differentially expressed important candidate genes in parental strains in the QTL region are relevant to myeloid cell, apoptotic activities, or to both. About one-quarter of those genes have been previously linked to arthritis in literature. The present study reveals two distinct subpopulations of arthritic mice with spontaneous arthritis due to deficiency for interleukin-1 receptor antagonist, suggesting that genes with function relevant to myeloid cell and/or apoptotic activities are most likely the key candidate genes for the QTL.

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