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

Jin, Hye-Mi; Kim, Tae‐Jong; Choi, Jung‐Ho; Kim, Moon‐Ju; Cho, Young-Nan; Nam, Kwang Il; Kee, Seung‐Jung; Moon, Jang Bae; Choi, Seok‐Yong; Park, Dong-Jin; Lee, Shin-Seok; Park, Yong-Wook

doi:10.1186/ar4531

Cited by 76 publications

(79 citation statements)

References 30 publications

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“…Several in vivo and in vitro studies reported that silencing miR-155 could ameliorate the disease severity and delay the onset of experimental autoimmune encephalomyelitis (EAE) and RA (9)(10)(11)(12). Additionally, miR-155 was found dysregulated in splenocytes from SLE-prone mice as compared with age-matched controls and was closely related to SLE susceptibility (13).…”

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confidence: 99%

miR-155 Deficiency Ameliorates Autoimmune Inflammation of Systemic Lupus Erythematosus by Targeting S1pr1 in Faslpr/lpr Mice

Xin

Deng

et al. 2015

The Journal of Immunology

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MicroRNA-155 (miR-155) was previously found involved in the development of systemic lupus erythematosus (SLE) and other autoimmune diseases and the inflammatory response; however, the detailed mechanism of miR-155 in SLE is not fully understood. To explore the in vivo role of miR-155 in the pathogenesis of SLE, miR-155–deficient Faslpr/lpr (miR-155−/−Faslpr/lpr) mice were obtained by crossing miR-155−/− and Faslpr/lpr mice. Clinical SLE features such as glomerulonephritis, autoantibody levels, and immune system cell populations were compared between miR-155−/−Faslpr/lpr and Faslpr/lpr mice. Microarray analysis, RT-PCR, Western blot, and luciferase reporter gene assay were used to identify the target gene of miR-155. miR-155−/−Faslpr/lpr mice showed milder SLE clinical features than did Faslpr/lprmice. As compared with Faslpr/lpr mice, miR-155−/−Faslpr/lpr mice showed less deposition of total IgA, IgM, and IgG and less infiltration of inflammatory cells in the kidney. Moreover, the serum levels of IL-4 and IL-17a, secreted by Th2 and Th17 cells, were lower in miR-155−/−Faslpr/lpr than Faslpr/lpr mice; the CD4+/CD8+ T cell ratio was restored in miR-155−/−Faslpr/lpr mice as well. Sphingosine-1-phosphate receptor 1 (S1PR1) was found as a new target gene of miR-155 by in vitro and in vivo studies; its expression was decreased in SLE patients and Faslpr/lpr mice. miR-155−/−Faslpr/lpr mice are resistant to the development of SLE by the regulation of the target gene S1pr1. miR-155 might be a new target for therapeutic intervention in SLE.

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confidence: 99%

miR-155 Deficiency Ameliorates Autoimmune Inflammation of Systemic Lupus Erythematosus by Targeting S1pr1 in Faslpr/lpr Mice

Xin

Deng

et al. 2015

The Journal of Immunology

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“…miR-155, an oncogenic miRNA, is identified as a link between inflammation and cancer (14). Previous studies have found that miR-155 expression is induced by proinflammatory mediators, such as TnF-α and LPS (15), and overexpression of miR-155 has been found to elevate inflammatory cytokine production in intestinal myofibroblasts (16) and monocyte/macrophages (17,18). In addition, some studies indicate that the promoter region of pri-miR-155 contains putative NF-κB-binding sites (19,20) and miR-155 upregulation and subsequent molecular events are associated with inflammatory processes such as activation of nF-κB (21,22).…”

Section: Introductionmentioning

confidence: 99%

S100A8 facilitates the migration of colorectal cancer cells through regulating macrophages in the inflammatory microenvironment

Zha

Sun

et al. 2016

Oncology Reports

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Abstract.Previous studies have shown that S100 calcium-binding protein A8 (S100A8) contributes to the survival and migration of colorectal cancer (CRC) cells. However, whether S100A8 participates in the progression and metastasis of CRC via the regulation of macrophages in the tumor inflammatory microenvironment remains unknown. In this study, phorbol myristate acetate (PMA) was used to induce the differentiation of THP-1 monocytes to macrophages. MTT assay, western blot analysis, immunofluorescence staining, semi-quantitative RT-PCR (semi-PCR), quantitative real-time PCR (qPCR), Gaussia luciferase activity assay and ELISA were performed to analyze the roles and molecular mechanisms of S100A8 in the modulation of macrophages. MTT assay, flow cytometric analysis, Hoechst staining, wound healing and Transwell migration assay were used to test the effect of S100A8 on the viability and migration of CRC cells co-cultured with macrophages in the inflammatory microenvironment. We found that THP-1 monocytes were induced by PMA and differentiated to macrophages. S100A8 activated the NF-κB pathway in the macrophages and promoted the expression of miR-155 and inflammatory cytokines IL-1β and TNF-α in the inflammatory microenvironment mimicked by lipopolysaccharides (LPS). Furthermore, S100A8 contributed to augment the migration but not the viability of the CRC cells co-cultured with the macrophages in the inflammatory microenvironment. Altogether, our study demonstrated that S100A8 facilitated the migration of CRC cells in the inflammatory microenvironment, and the underlying molecular mechanisms may be partially attributed to the overexpression of miR-155, IL-1β and TNF-α through activation of the NF-κB pathway in macrophages. IntroductionColorectal cancer (CRC), for which distant metastasis accounts for the leading cause of cancer mortality, is one of the most malignant gastrointestinal carcinomas worldwide (1). The pathogenesis of CRC is a complex process and involves environmental influences, genetic alterations, and the host immune system and their interactions. The formation of an inflammatory microenvironment also plays a pivotal role in the development of CRC (2). The host microenvironment is comprised of numerous infiltrating immune cell types and resident tumor cells. Among the immune cells, macrophages play an indispensable role. For instance, macrophage infiltration in colon tissue has been observed in both inflammatory bowel disease (IBD) and CRC (4), and the cytokines secreted by macrophages under certain conditions have directly or indirectly stimulated inflammation and tumor progression (5,6). Although great progress has been made, the interactions and the molecular mechanisms between CRC and the inflammatory microenvironment remain unknown. S100A8 (calgranulin A or S100 calcium-binding protein A8) is a member of the low-molecular calcium binding S100 protein family. It also belongs to the family of damage-associated molecular patterns (DAMPs). Studies have shown that S100A8 plays an important role in regul...

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“…Over 5000 miRNAs have now been identified, and miRNAs play an important role in a wide range of human diseases, including cancer, metabolic diseases, and inflammatory diseases. Recent studies suggested that miRNAs may be involved in the development of inflammatory arthritis, including acute gouty arthritis [5,6]. The miRNAs mainly bind to the 3′-untranslated regions (3'UTR) of target mRNAs, resulting in mRNA degradation or the inhibition of mRNA translation [10].…”

Section: Overview Of Mirnasmentioning

confidence: 99%

“…miRNAs play an important role in human diseases, including some inflammatory diseases. Recent studies suggested that miRNAs may be involved in the development of inflammatory arthritis, including acute gouty arthritis [5,6]. In resent review, we will systemically review relevant literatures to get a better understanding on the possible roles of miRNAs in gout.…”

Section: Introductionmentioning

confidence: 99%

Could MicroRNAs be Regulators of Gout Pathogenesis?

Wang¹,

Xu²,

Wang³

et al. 2015

Cell Physiol Biochem

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MicroRNAs (miRNAs) are a class of noncoding RNAs that mainly negatively regulate gene expression. miRNAs have important roles in many diseases, including inflammatory diseases. Gout is a common arthritis caused by deposition of monosodium urate crystals within joints. Recent studies suggested that miRNAs may be involved in the development of inflammatory arthritis, including acute gouty arthritis. In the present review, we systemically discuss relevant publications in order to provide a better understanding on the possible role of miRNAs in gout. miRNAs may act as regulators of gout pathogenesis via several pathways. Targeting miRNAs may be a promisingstrategy in the treatment of gout.

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

Cited by 76 publications

References 30 publications

miR-155 Deficiency Ameliorates Autoimmune Inflammation of Systemic Lupus Erythematosus by Targeting S1pr1 in Faslpr/lpr Mice

miR-155 Deficiency Ameliorates Autoimmune Inflammation of Systemic Lupus Erythematosus by Targeting S1pr1 in Faslpr/lpr Mice

S100A8 facilitates the migration of colorectal cancer cells through regulating macrophages in the inflammatory microenvironment

Could MicroRNAs be Regulators of Gout Pathogenesis?

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