miR-22 inhibits synovial fibroblasts proliferation and proinflammatory cytokine production in RASF via targeting SIRT1

Zhang, Chengqiang; Fang, Lihua; Li, Xiaoping; Tang, Nujiang; Li, Rui; Cui, Liangyu; Wang, Jie; Ji, Yanhong

doi:10.1016/j.gene.2019.144144

Cited by 25 publications

(10 citation statements)

References 39 publications

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“…Beyond miR-217 and miR-34a, other miRNAs are also known to regulate SIRT1 [29]. MiR-128-3p, miR-miR-9, MicroRNA-29a and miR-22all can reducedSIRT1 expression and exacerbated the inflammatory response [30][31][32][33]. However; their roles in the development of ALD will need to be further investigated.…”

Section: Ivyspring International Publishermentioning

confidence: 99%

Emerging Roles of SIRT1 in Alcoholic Liver Disease

Ren¹,

Wang²,

Wu³

et al. 2020

Int. J. Biol. Sci.

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Alcoholic liver disease (ALD) is the most prevalent type of chronic liver disease worldwide with a wide spectrum of liver pathologies ranging from simple steatosis to steatohepatitis, cirrhosis, and even hepatocellular carcinoma. It has been demonstrated that ALD is mediated in whole or in part by a central signaling molecule sirtuin 1 (SIRT1), a conserved class III histone deacetylase.SIRT1 plays beneficial roles in regulating hepatic lipid metabolism, inhibiting hepatic inflammation, controlling hepatic fibrosis and mediating hepatocellular carcinoma in ALD. However, underlying molecular mechanisms are complex and remain incompletely understood. The aim of this review was to highlight the latest advances in understanding of SIRT1 regulatory mechanisms in ALD and discuss their unique potential role as novel therapeutic target for ALD treatment.

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Section: Ivyspring International Publishermentioning

confidence: 99%

Emerging Roles of SIRT1 in Alcoholic Liver Disease

Ren¹,

Wang²,

Wu³

et al. 2020

Int. J. Biol. Sci.

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“…Synovial tissue is an important part of the knee joint, which mostly includes synovial macrophages and fibroblast-like synoviocytes (FLS) (95); synoviocyte proliferation, invasion, and migration are essential for the RA pathology (96). Among synovial and FLS miRNAs, miR-21 (39), miR-26a-5p (41), miR-126 (50), miR-135a (51), miR-138 (54), miR-143 (56), miR-145 (56), miR-155 (58), and miR-421 (63) are overexpressed, whereas miR-19a (37), miR-20a (38), miR-22 (40), miR-27a (42), miR-29a (44), miR-34a (45), miR-137 (53), miR-140-3p (55), miR−152 (57), and miR-495 (68) are downregulated. The disturbed miRNAs enhance the expression level of proinflammatory cytokine (IL-6, IL-8, TNF-a, and IL-1b) and enzymes that erode the bone matrix (MMP-1 and MMP-3) by affecting Wnt (97,98), NF-kB (81,99), JAK/STAT (48,100), and TLR (101,102) pathways.…”

Section: Introductionmentioning

confidence: 99%

Functional Interactions Between lncRNAs/circRNAs and miRNAs: Insights Into Rheumatoid Arthritis

2022

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Rheumatoid arthritis (RA) is one of the most common autoimmune diseases that affect synovitis, bone, cartilage, and joint. RA leads to bone and cartilage damage and extra-articular disorders. However, the pathogenesis of RA is still unclear, and the lack of effective early diagnosis and treatment causes severe disability, and ultimately, early death. Accumulating evidence revealed that the regulatory network that includes long non-coding RNAs (lncRNAs)/circular RNAs (circRNAs), micro RNAs (miRNAs), and messenger RNAs (mRNA) plays important roles in regulating the pathological and physiological processes in RA. lncRNAs/circRNAs act as the miRNA sponge and competitively bind to miRNA to regulate the expression mRNA in synovial tissue, FLS, and PBMC, participate in the regulation of proliferation, apoptosis, invasion, and inflammatory response. Thereby providing new strategies for its diagnosis and treatment. In this review, we comprehensively summarized the regulatory mechanisms of lncRNA/circRNA-miRNA-mRNA network and the potential roles of non-coding RNAs as biomarkers and therapeutic targets for the diagnosis and treatment of RA.

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“…Acute inflammatory stimulus promoted the expression of anti-inflammatory mediators including PPAR- γ and SIRT1 to quench the flame. However, this attempt may fail under intense inflammation, because their mRNA can be destabilized ( Jennewein et al, 2010 ; Zhang et al, 2019 ). Once again, we noticed that the levels of SIRT1, PPAR- γ and SCD-1 were increased by MAN.…”

Section: Resultsmentioning

confidence: 99%

α-Mangostin Alleviated Inflammation in Rats With Adjuvant-Induced Arthritis by Disrupting Adipocytes-Mediated Metabolism-Immune Feedback

Han

Wang

et al. 2021

Front. Pharmacol.

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A previously identified anti-rheumatic compound α-mangostin (MAN) possesses notable metabolism regulatory properties. In this study, we investigated the immune implication of MAN-altered fat metabolism on adjuvant-induced arthritis (AIA) in rats. Seven days after AIA induction, the rats received oral treatment of MAN at 50 mg/kg/day for 30 days. Metabolic indicators and basic clinical parameters were evaluated using samples collected on day 20 and 38 since immunization. Expression of nicotinamide phosphoribosyltransferase (NAMPT), sirtuin 1 (SIRT1), peroxisome proliferator activated receptor gamma (PPAR-γ), stearoyl-coa desaturase 1 (SCD-1), toll like receptor 4 (TLR4), prostaglandin-endoperoxide synthase 2 (COX-2), (p)-JNK, (p)-p65 and IL-1β were investigated by either RT-qPCR or immunobloting methods. In in vitro experiments, we treated (pre)-adipocytes with monocytes/macrophages and MAN, and investigated the changes of macrophages brought by pre-adipocytes co-culture. Generally, MAN restored the impaired fat anabolism in AIA rats, indicated by increased fat reservoir, leptin and adiponectin secretion, and PPAR-γ and SCD-1 expression. Meanwhile, it decreased circulating IL-1β and IL-6 levels, restored serological lipid profile changes, and relieved oxidative stresses, demonstrating potent therapeutic effects on AIA. AIA rats-derived monocytes inhibited mRNA PPAR-γ and SCD-1 expression in pre-adipocytes. Contrarily, MAN facilitated adipocyte differentiation in vitro, and increased free fatty acids production. It also significantly increased PPAR-γ and SCD-1 expression, which can be abrogated by PPAR-γ inhibitor T0070907. Similarly, lipopolysaccharide-primed macrophages inhibited PPAR-γ expression in the co-cultured pre-adipocytes, which was reversed by MAN. In the same co-culture system, lipopolysaccharide-induced inflammation was amplified by the co-existence of pre-adipocytes. More secretion of IL-1β and IL-6 and higher levels expression of COX-2, p-JNK, p-p65 and TLR4 were observed in lipopolysaccharide-treated macrophages when co-cultured by pre-adipocytes. The intensified inflammatory situation was eased by MAN. The treatment with pre-adipocytes culture medium achieved similar effects. Medium from lipopolysaccharide-treated adipocytes promoted IL-1β, IL-6 and MCP-1 production in separately cultured macrophages, and COX-2, p-JNK, p-p65 and TLR4 expression were increased at the meantime. MAN treatment on pre-adipocytes impaired these changes. It suggests that fat anabolism in AIA rats was deficient due to increased energy expenditure caused by inflammatory conditions. MAN restored fat metabolism homeostasis by up-regulating PPAR-γ, and reshaped secretion profile of adipocytes.

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miR-22 inhibits synovial fibroblasts proliferation and proinflammatory cytokine production in RASF via targeting SIRT1

Cited by 25 publications

References 39 publications

Emerging Roles of SIRT1 in Alcoholic Liver Disease

Emerging Roles of SIRT1 in Alcoholic Liver Disease

Functional Interactions Between lncRNAs/circRNAs and miRNAs: Insights Into Rheumatoid Arthritis

α-Mangostin Alleviated Inflammation in Rats With Adjuvant-Induced Arthritis by Disrupting Adipocytes-Mediated Metabolism-Immune Feedback

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