Nesfatin-1 facilitates IL-1β production in osteoarthritis synovial fibroblasts by suppressing miR-204-5p synthesis through the AP-1 and NF-κB pathways

Lee, Kun-Tsan; Chen, Bo-Cheng; Liu, Shan‐Chi; Lin, Yen‐You; Tsai, Cheng-Han; Ko, Chih‐Yuan; Tang, Chih‐Hsin; Tung, Kwong‐Chung

doi:10.18632/aging.203559

Cited by 11 publications

(8 citation statements)

References 58 publications

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“…Studies have demonstrated that NF-κB is a key member of lipocalin 2-induced OA ( Guo et al, 2014 ; Conde et al, 2016 ). A novel adipokine, Nesfatin-1, was also found to stimulate NF-κB pathway ( Lee et al, 2021 ).…”

Section: Adipokine Signaling Pathways In Osteoarthritismentioning

confidence: 99%

Adipokine Signaling Pathways in Osteoarthritis

Zhang

Lin

Yan

et al. 2022

Front. Bioeng. Biotechnol.

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Osteoarthritis (OA) is a debilitating joint disease that affects millions of individuals. The pathogenesis of OA has not been fully elucidated. Obesity is a well-recognized risk factor for OA. Multiple studies have demonstrated adipokines play a key role in obesity-induced OA. Increasing evidence show that various adipokines may significantly affect the development or clinical course of OA by regulating the pro/anti-inflammatory and anabolic/catabolic balance, matrix remodeling, chondrocyte apoptosis and autophagy, and subchondral bone sclerosis. Several signaling pathways are involved but still have not been systematically investigated. In this article, we review the cellular and molecular mechanisms of adipokines in OA, and highlight the possible signaling pathways. The review suggested adipokines play important roles in obesity-induced OA, and exert downstream function via the activation of various signaling pathways. In addition, some pharmaceuticals targeting these pathways have been applied into ongoing clinical trials and showed encouraging results. However, these signaling pathways are complex and converge into a common network with each other. In the future work, more research is warranted to further investigate how this network works. Moreover, more high quality randomised controlled trials are needed in order to investigate the therapeutic effects of pharmaceuticals against these pathways for the treatment of OA. This review may help researchers to better understand the pathogenesis of OA, so as to provide new insight for future clinical practices and translational research.

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Section: Adipokine Signaling Pathways In Osteoarthritismentioning

confidence: 99%

Adipokine Signaling Pathways in Osteoarthritis

Zhang

Lin

Yan

et al. 2022

Front. Bioeng. Biotechnol.

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“…Controversy surrounds nesfatin-1 in arthritis diseases, as this adipokine exhibits both proinflammatory and anti-inflammatory functions. For example, nesfatin-1 can suppress IL-1β expression in OA chondrocytes and thus reduce the severity of cartilage destruction in OA rats 39 , but nesfatin-1 can also facilitate IL-1β expression in OA synovial fibroblasts 40 . Interestingly, nesfatin-1 shows protective effects in cartilage from rats with adjuvant-induced arthritis 41 and reportedly reduces the risk of atherosclerotic disease in patients with RA 42 .…”

Section: Discussionmentioning

confidence: 99%

Nesfatin-1 Stimulates CCL2-dependent Monocyte Migration And M1 Macrophage Polarization: Implications For Rheumatoid Arthritis Therapy

Chang¹,

Liu²,

Lin³

et al. 2023

Int. J. Biol. Sci.

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Rheumatoid arthritis (RA) is a prototypic inflammatory disease, characterized by the infiltration of proinflammatory cytokines into the joint synovium and the migration of mononuclear cells into inflammatory sites. The adipokine nesfatin-1 is linked to inflammatory events in various diseases, although its role in RA pathology is uncertain. Analysis of the Gene Expression Omnibus GSE55235 dataset revealed high levels of expression of the adipokine nesfatin-1 in human RA synovial tissue. Similarly, our human synovial tissue samples exhibited increasing levels of nesfatin-1 expression and Ccl2 mRNA expression. Nesfatin-1-induced stimulation of CCL2 expression and monocyte migration involved the MEK/ERK, p38, and NF-κB signaling pathways. Notably, nesfatin-1-induced increases in CCL2 expression favored M1 macrophage polarization, which increased the expression of proinflammatory cytokines IL-1β, IL-6, and TNF-α. Finally, nesfatin-1 shRNA ameliorated the severity of inflammatory disease and reduced levels of M1 macrophage expression in CIA mice. Our studies confirm that nesfatin-1 appears to be worth targeting in RA treatment.

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“…Controversy surrounds nesfatin-1 in arthritis diseases, as this adipokine exhibits both proin ammatory and anti-in ammatory functions. For example, nesfatin-1 can suppress IL-1β expression in OA chondrocytes and thus reduce the severity of cartilage destruction in OA rats (34), but nesfatin-1 can also facilitate IL-1β expression in OA synovial broblasts (35). Interestingly, nesfatin-1 shows protective effects in cartilage from rats with adjuvant-induced arthritis(36) and reportedly reduces the risk of atherosclerotic disease in patients with RA (37).…”

Section: Discussionmentioning

confidence: 99%

Nesfatin-1 stimulates CCL2-dependent monocyte migration and M1 macrophage polarization: implications for rheumatoid arthritis therapy

Chang¹,

Liu²,

Lin³

et al. 2022

Preprint

Self Cite

View full text Add to dashboard Cite

Rheumatoid arthritis (RA) is a prototypic inflammatory disease, characterized by the infiltration of proinflammatory cytokines into the joint synovium and the migration of mononuclear cells into inflammatory sites. The adipokine nesfatin-1 is linked to inflammatory events in various diseases, although its role in RA pathology is uncertain. Analysis of the Gene Expression Omnibus GSE55235 dataset revealed high levels of expression of the adipokine nesfatin-1 in human RA synovial tissue. Similarly, our human synovial tissue samples exhibited increasing levels of nesfatin-1 expression and Ccl2 mRNA expression. Nesfatin-1-induced stimulation of CCL2 expression and monocyte migration involved the MEK/ERK, p38 and NF-κB signaling pathways. Notably, nesfatin-1-induced increases in CCL2 expression favored M1 macrophage polarization, which increased the expression of proinflammatory cytokines IL-1β, IL-6 and TNF-α. Finally, nesfatin-1 shRNA ameliorated the severity of inflammatory disease and reduced levels of M1 macrophage expression in CIA mice. Our studies confirms that nesfatin-1 appears to be worth targeting in RA treatment.

show abstract

Nesfatin-1 facilitates IL-1β production in osteoarthritis synovial fibroblasts by suppressing miR-204-5p synthesis through the AP-1 and NF-κB pathways

Cited by 11 publications

References 58 publications

Adipokine Signaling Pathways in Osteoarthritis

Adipokine Signaling Pathways in Osteoarthritis

Nesfatin-1 Stimulates CCL2-dependent Monocyte Migration And M1 Macrophage Polarization: Implications For Rheumatoid Arthritis Therapy

Nesfatin-1 stimulates CCL2-dependent monocyte migration and M1 macrophage polarization: implications for rheumatoid arthritis therapy

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