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MicroRNA-155 as a proinflammatory regulator via SHIP-1 down-regulation in acute gouty arthritis
Introduction:
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.
Methods:
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.
Results:
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.
Conclusions:
Overexpression of miR-155 in the gouty SFMC leads to suppress SHIP-1 levels and enhance proinflammatory cytokines.
Insights
MicroRNA-155 (miR-155) plays a key role in gouty arthritis by increasing inflammatory cytokines and decreasing SHIP-1 levels. This study clarifies miR-155's function in gout pathogenesis.
Area of Science:
- Immunology
- Molecular Biology
- Rheumatology
Background:
- Gout is a painful inflammatory arthritis caused by monosodium urate (MSU) crystals.
- MicroRNA-155 (miR-155) is known to be important in myeloid cell activation and inflammatory arthritis.
- The specific role of miR-155 in acute gouty arthritis was previously undefined.
Purpose of the Study:
- To investigate the role of miR-155 in the pathogenesis of acute gouty arthritis.
- To determine the relationship between miR-155, SHIP-1, and inflammatory cytokine production in gout.
Main Methods:
- Collected samples from gout patients and healthy controls.
- Cultured peripheral blood mononuclear cells (PBMCs) and synovial fluid mononuclear cells (SFMCs) with MSU crystals.
- Assessed gene expression of miR-155 and SHIP-1 using real-time PCR.
- Measured inflammatory cytokine levels (TNF-α, IL-1β) via Luminex.
- Utilized a mouse model of gout to analyze miR-155, SHIP-1, and cytokine expression.
Main Results:
- miR-155 expression was significantly elevated in gout samples compared to healthy controls.
- MSU crystal stimulation strongly induced miR-155 expression in vitro.
- Overexpression of miR-155 led to decreased SHIP-1 levels and increased production of pro-inflammatory cytokines (TNF-α, IL-1β).
- Elevated miR-155 and inflammatory cytokine production were observed in a mouse model of gout.
Conclusions:
- miR-155 overexpression in gouty synovial fluid mononuclear cells suppresses SHIP-1 levels.
- miR-155 enhances the production of pro-inflammatory cytokines, contributing to gout pathogenesis.
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