ORIGINAL ARTICLE

Beta 2-microglobulin amyloid deposit in HLA-B27 transgenic rats

Authors

Shigeo Fukunishi¹, Kohsei Yoh¹, Seiya Kamae¹ and Shinichi Yoshiya¹

1. Department of Orthopaedic Surgery, Hyogo college of Medicine, 1-1 Mukogawa-cho, Nishinomiya 663-8501, Japan

Received:

18 January 2007

Accepted:

22 May 2007

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Abstract

Beta 2-microglobulin (beta 2-m) amyloid deposition develops serious orthopedic complications in patients with long-term hemodialysis. However, the exact pathogenesis of amyloid deposition in patients with dialysis is unknown. We used transgenic rats with HLA-B27 and beta 2-m to develop an in vivo animal model with beta 2-m amyloid-associated disorders to investigate the mechanism of formation and to report histological findings of beta 2-m amyloid deposition. Transgenic rats were divided into two groups: group 1, no treatment; group 2, arthritis induced by type II collagen. A large number of cells labeled with beta 2-m were observed in the bone marrow and synovium of the knee joint in transgenic rats. In addition, amyloid deposition, identified by Congo red staining, was found only in the knee joints of the transgenic rats with collagen-induced arthritis. Immunostaining with beta 2-m demonstrated the same pattern of tissue distribution as Congo red in serial sections. We hypothesized that elevated serum beta 2-m level-associated local chronic inflammation leads to the development of amyloid deposits and resultant arthropathy.

Key words

Amyloid - Beta 2-microglobulin - Hemodialysis - HLA-B27 transgenic rats