Associations between Adipokines in Arthritic Disease and Implications for Obesity

MacDonald, Iona; Liu, Shan‐Chi; Huang, Chien-Chung; Kuo, Sheng‐Fong; Tsai, Chun‐Hao; Tang, Chih‐Hsin

doi:10.3390/ijms20061505

Cited by 54 publications

(42 citation statements)

References 106 publications

(139 reference statements)

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“…However, its underlying mechanism remains unknown, and thus, its treatment is a challenge. So far, many studies have explored the association between adipokine, obesity, and OA [32][33][34]. For instance, leptin has been found to be significantly increased in OA patients [35] and it has catabolic and proinflammatory effects in chondrocytes [36].…”

Section: Discussionmentioning

confidence: 99%

Nesfatin-1 suppresses interleukin-1β-induced inflammation, apoptosis, and cartilage matrix destruction in chondrocytes and ameliorates osteoarthritis in rats

Jiang

Zhou

et al. 2020

Aging

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Osteoarthritis (OA) is a chronic degenerative joint disease, related to the overexpression of matrix metalloproteinases (MMPs), a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS), inflammation, and chondrocyte apoptosis. Nesfatin-1 is an adipokine, which plays an important role in the development of OA, especially in obese people. In the present study, cartilage degradation and apoptosis observed in OA patients was evaluated. Furthermore, the anti-inflammatory and anti-apoptotic effects of nesfatin-1, and its underlying in vitro and in vivo mechanisms were investigated. The results showed that nesfatin-1 increased significantly the expression of collagen type II alpha 1 chain (Col2a1), and reduced the expression of MMPs, ADAMTS5, cyclooxygenase (COX)-2, caspase-3, nitric oxide (NO), inducible nitric oxide synthase (iNOS), prostaglandin E2 (PGE2), interleukin (IL)-6, and chondrocyte apoptosis rate, which may be induced by IL-1β in rat chondrocytes. Furthermore, nesfatin-1 treatment prevented cartilage degeneration in the rat OA model. It was found that nesfatin-1 suppressed the IL-1β-induced activation of NF-κB, the mitogen-activated protein kinase (MAPK), and the Bax/Bcl-2 signal pathway in chondrocytes. These results suggest that in vivo nesfatin-1 could play a protective role in the development of OA and can be potentially used for its treatment.

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Section: Discussionmentioning

confidence: 99%

Nesfatin-1 suppresses interleukin-1β-induced inflammation, apoptosis, and cartilage matrix destruction in chondrocytes and ameliorates osteoarthritis in rats

Jiang

Zhou

et al. 2020

Aging

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“…Adipokines are adipose tissue‐secreted cytokines that regulate multiple cellular functions such as progression, migration and inflammation 30 . Some adipokines are critical in the pathogenesis of rheumatoid arthritis (RA) and OA 31 . Adiponectin increases levels of IL‐6 expression and oncostatin M production in human RA and OA synovial fibroblasts 32,33 .…”

Section: Discussionmentioning

confidence: 99%

Resistin enhances IL‐1β and TNF‐α expression in human osteoarthritis synovial fibroblasts by inhibiting miR‐149 expression via the MEK and ERK pathways

Chen

Kuo

et al. 2020

FASEB j.

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Resistin is a cysteine‐rich adipokine that promotes the release of inflammatory cytokines, particularly interleukin 1 beta (IL‐1β) and tumor necrosis factor alpha (TNF‐α), which are critical pro‐inflammatory mediators in osteoarthritis (OA) pathogenesis. We describe evidence of significantly higher levels of resistin, IL‐1β, and TNF‐α expression in OA knee synovial tissue compared with that from non‐OA knees. Resistin‐induced enhancement of IL‐1β and TNF‐α expression in human OA synovial fibroblasts (OASFs) were attenuated by MEK and ERK inhibitors, as well as their respective siRNAs. Our data reveal that resistin enhances the expression of TNF‐α and IL‐1β in OASFs by inhibiting miR‐149 expression via MEK and ERK signaling. Our findings elucidate the inter‐relationships between resistin and pro‐inflammatory mediators during OA pathogenesis and could help to facilitate the development of synovium‐targeted therapy in OA.

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“…However, despite the observations suggesting a correlation between obesity and OA, the detailed mechanisms underlying this correlation are far from clear. What is known is that adipokines, multifunctional molecules secreted by adipose tissue, act as an intersecting link between obesity and OA by modulating the activities of cartilage, synovium, bone, and various immune cells [3,7].…”

Section: Agingmentioning

confidence: 99%

Apelin enhances IL-1β expression in human synovial fibroblasts by inhibiting miR-144-3p through the PI3K and ERK pathways

Chang

Wang

Kuo

et al. 2020

Aging

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Associations between Adipokines in Arthritic Disease and Implications for Obesity

Cited by 54 publications

References 106 publications

Nesfatin-1 suppresses interleukin-1β-induced inflammation, apoptosis, and cartilage matrix destruction in chondrocytes and ameliorates osteoarthritis in rats

Nesfatin-1 suppresses interleukin-1β-induced inflammation, apoptosis, and cartilage matrix destruction in chondrocytes and ameliorates osteoarthritis in rats

Resistin enhances IL‐1β and TNF‐α expression in human osteoarthritis synovial fibroblasts by inhibiting miR‐149 expression via the MEK and ERK pathways

Apelin enhances IL-1β expression in human synovial fibroblasts by inhibiting miR-144-3p through the PI3K and ERK pathways

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