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MicroRNA-155 as a proinflammatory regulator via SHIP-1 down-regulation in acute gouty arthritis

Hye Mi Jin1, Tae-Jong Kim1*, Jung-Ho Choi1, Moon-Ju Kim1, Young-Nan Cho1, Kwang-Il Nam2, Seung-Jung Kee3, Jang Bae Moon4, Seok-Yong Choi5, Dong-Jin Park1, Shin-Seok Lee1 and Yong-Wook Park1

Author Affiliations

1 Department of Rheumatology, Research Institute of Medical Sciences, Chonnam National University Medical School and Hospital, 671 Jebongro, Dong-gu, Gwangju 501-757, Republic of Korea

2 Department of Anatomy, Chonnam National University Medical School, 160 Baekseo-ro, Gwangju 501-840, South Korea

3 Department of Laboratory Medicine, Chonnam National University Medical School and Hospital, 42, Jebong-ro, Gwangju 501-757, South Korea

4 National Research Laboratory for Regulation of Bone Metabolism and Disease, Medical Research Center for Gene Regulation, Chonnam National University Medical School, 42, Jebong-ro, Gwangju 501-757, South Korea

5 Department of Biomedical Sciences, Chonnam National University Medical School, Gwangju, Republic of Korea

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Arthritis Research & Therapy 2014, 16:R88  doi:10.1186/ar4531

Published: 7 April 2014



Gout is characterized by episodes of intense joint inflammation in response to intra-articular monosodium urate monohydrate (MSU) crystals. miR-155 is crucial for the proinflammatory activation of human myeloid cells and antigen-driven inflammatory arthritis. The functional role of miR-155 in acute gouty arthritis has not been defined. Therefore, the aim of this study was to examine the role of miR-155 in pathogenesis of acute gouty arthritis.


Samples from 14 patients with acute gouty arthritis and 10 healthy controls (HCs) were obtained. Peripheral blood mononuclear cells (PBMCs) and synovial fluid mononuclear cells (SFMCs) were cultured in vitro with MSU crystals, and gene expression (human miR-155 and SHIP-1) were assessed by real-time PCR. THP-1 cells were stimulated by MSU crystals and/or miR-155 transfection and then subjected to Western blot analysis. Levels of human tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-1β in cell culture supernatants were measured by Luminex. Immunohistochemistry was performed on formalin-fixed gout tissues with anti–SHIP-1 antibody. A C57BL/6 J male mouse model of gout was used to analyze the expressions of miR-155, SHIP-1, and inflammatory cytokines.


The samples from gouty arthritis were highly enriched in miR-155, with levels of expression being higher than those found in PBMC from HC. Treatment of the cells with MSU crystals strongly induced miR-155. In addition, overexpression of miR-155 in the cells decreased levels of SHIP-1 and promoted production of MSU-induced proinflammatory cytokines, such as TNF-α and IL-1β. Consistent with in vitro observations, miR-155 expression was elevated in the mouse model of gout. The production of inflammatory cytokines was markedly increased in MSU crystal induced peritonitis mice.


Overexpression of miR-155 in the gouty SFMC leads to suppress SHIP-1 levels and enhance proinflammatory cytokines.