Monocyte chemoattractant protein 1 induced chondrocytes degeneration and cartilage degradation in osteoarthritis

yuankun, X.; Yan, Kaige; Bin, Wan; JianHao, Lin

doi:10.1016/j.joca.2016.01.275

Cited by 6 publications

(6 citation statements)

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“…Increased overall synovial fluid MCP-1 concentrations in OA, concomitant with clinical signs of joint inflammation, is consistent with the literature (82)(83)(84). During synovial inflammation, MCP-1 contributes to recruitment and accumulation of circulating monocytes in the synovial membrane (76,85).…”

Section: Cd14/cd186/cd206/il10 Expression (Macrophage Activation)supporting

confidence: 91%

Macrophage Activation in the Synovium of Healthy and Osteoarthritic Equine Joints

et al. 2020

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Synovitis is a major component of osteoarthritis and is driven primarily by macrophages. Synovial macrophages are crucial for joint homeostasis (M2-like phenotype), but induce inflammation (M1-like) when regulatory functions become overwhelmed. Macrophage phenotypes in synovium from osteoarthritic and healthy joints are poorly characterized; however, comparative knowledge of their phenotypes during health and disease is paramount for developing targeted treatments. This study compared patterns of macrophage activation in healthy and osteoarthritic equine synovium and correlated histology with cytokine/chemokine profiles in synovial fluid. Synovial histology and immunohistochemistry for M1-like (CD86), M2-like (CD206, IL-10), and pan macrophage (CD14) markers were performed on biopsies from 29 healthy and 26 osteoarthritic equine joints. Synovial fluid cytokines (MCP-1, IL-10, PGE2, IL-1β, IL-6, TNF-α, IL-1ra) and growth factors (GM-CSF, SDF-1α+β, IGF-1, and FGF-2) were quantified. Macrophage phenotypes were not as clearly defined in vivo as they are in vitro. All macrophage markers were expressed with minimal differences between OA and normal joints. Expression for all markers increased proportionate to synovial inflammation, especially CD86. Synovial fluid MCP-1 was higher in osteoarthritic joints while SDF-1 and IL-10 were lower, and PGE2 concentrations did not differ between groups. Increased CD14/CD86/CD206/IL-10 expression was associated with synovial hyperplasia, consistent with macrophage recruitment and activation in response to injury. Lower synovial fluid IL-10 could suggest that homeostatic mechanisms from synovial macrophages became overwhelmed preventing inflammation resolution, resulting in chronic inflammation and OA. Further investigations into mechanisms of arthritis resolution are warranted. Developing pro-resolving therapies may provide superior results in the treatment of OA.

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Section: Cd14/cd186/cd206/il10 Expression (Macrophage Activation)supporting

confidence: 91%

Macrophage Activation in the Synovium of Healthy and Osteoarthritic Equine Joints

et al. 2020

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“…Increased overall synovial fluid MCP-1 in OA concomitant with gross signs of inflammation and clinical signs is consistent with the literature (76)(77)(78). During synovial inflammation, MCP-1 contributes to recruitment, homing, and accumulation of mononuclear cells in the synovial fluid and membrane (68,79), as part of the homeostatic response to joint damage (15).…”

Section: Intensity Of Expression Did Vary With Degree Of Synovial Infsupporting

confidence: 89%

Comparative analysis of macrophage activation in the synovium of healthy and osteoarthritic equine joints

Menarim

Gillis

Oliver

et al. 2020

Preprint

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Background: Synovitis is a major component of osteoarthritis and is driven primarily by macrophages. Synovial macrophages are crucial keepers of joint health by driving joint homeostasis, tissue repair and inflammation resolution (M2-like phenotype), but can also induce an inflammatory response (M1-like phenotype) when these regulatory functions are overwhelmed. Macrophage phenotypes in synovium from osteoarthritic and healthy joints are poorly characterized. Defining the patterns of synovial macrophage phenotypes in normal and osteoarthritic joints is paramount for developing targeted therapeutic approaches. The objective of this study was to compare patterns of macrophage activation phenotypes in healthy and osteoarthritic equine joints. We hypothesized that synovium from osteoarthritic joints would have increased M1-like:M2-like ratios compared to normal joints. Methods: Gross evaluation of the articular surfaces, histology (H&E) and immunohistochemistry for M1-like (CD86), M2-like (CD206, IL-10), and pan macrophage (CD14) markers was performed on synovial biopsies from healthy (n=29) and osteoarthritic equine joints (n=26). Cytokines (MCP-1, IL-10, PGE 2 , IL-1β, IL-6, TNF-α, IL-1ra) and growth factors (GM-CSF, SDF-1α+β, IGF-1, and FGF-2) in synovial fluid were quantified. Results: All macrophage markers were co-expressed in all joints with minimal differences between OA and normal joints. Intensity of expression varied with degree of synovial inflammation. CD14, CD86, CD206, and IL-10 were more highly expressed in grossly inflamed osteoarthritic synovium, with CD86 most highly expressed. Synovial fluid MCP-1 was higher in osteoarthritic joints while SDF-1 was lower. Overall, concentrations of synovial fluid IL-10 and PGE2 was not different between OA and normal joints. Increased CD14/CD86/CD206/Il-10 expression in the synovium was associated with synovial hyperplasia, consistent with macrophage recruitment and activation in response to higher demands for repair. Conclusions: Macrophages are not as clearly defined in vivo as they are in vitro . The course of an effective response to injury in joints should start with inflammation and be followed inflammation resolution, both of which centrally driven by macrophages. Combined, our findings suggest that homeostatic mechanisms from synovial macrophages are impaired in OA, resulting in unresolved, chronic joint inflammation. Therapeutic approaches aimed at recovering mechanisms of macrophage-driven synovial homeostasis may be more effective in treating osteoarthritis than simply inhibiting inflammation.

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“…33,43 Although TIMP-1 limits matrix degradation, TIMP-1 was analyzed because this protein has been shown to be increased in OA, 44,45 aging-related processes, 46,47 angiogenesis, 48 and fibrosis 49,50 -all of which are considered undesirable in OA. The inflammatory proteins IL-8, 51,52 VEGF, 53,54 and MCP-1 55,56 were selected because they have been demonstrated to exacerbate OA progression/ cartilage degradation. To help segment the study and aid in presentation of the results, the MMPs and TIMP-1 have been grouped together under "catabolic/OA markers" while the inflammatory proteins have been grouped together under "inflammation/OA markers."…”

Section: Concentration Of Osmolytesmentioning

confidence: 99%

Hyperosmolar Potassium (K⁺) Treatment Suppresses Osteoarthritic Chondrocyte Catabolic and Inflammatory Protein Production in a 3-Dimensional In Vitro Model

2017

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Objective The main goal of this study was to provide a proof-of-concept demonstrating that hyperosmolar K solutions can limit production of catabolic and inflammatory mediators in human osteoarthritic chondrocytes (OACs). Methods A 3-dimensional in vitro model with poly(ethylene glycol) diacrylate (PEGDA) hydrogels was used. Catabolic and pro-inflammatory protein production from encapsulated OACs was assessed following culture for 1 or 7 days in the presence or absence of 80 mM K gluconate, 80 mM sodium (Na) gluconate, or 160 mM sucrose, each added to culture media (final osmolarity ~490 mOsm). Results Relative to untreated controls, OACs treated with hyperosmolar (80 mM Na gluconate or 160 mM sucrose) solutions produced lower levels of catabolic and inflammatory mediators in a marker- and time-dependent manner (i.e., MMP-9 after 1 day; MCP-1 after 7 days ( P ≤ 0.015)). In contrast, OAC treatment with 80 mM K gluconate reduced catabolic and inflammatory mediators to a greater extent (both the number of markers and degree of suppression) relative to untreated, Na gluconate, or sucrose controls (i.e., MMP-3, -9, -13, TIMP-1, MCP-1, and IL-8 after 1 day; MMP-1, -3, -9, -13, TIMP-1, MCP-1, and IL-8 after 7 days ( P ≤ 0.029). Conclusions Hyperosmolar K solutions are capable of attenuating protein production of catabolic and inflammatory OA markers, providing the proof-of-concept needed for further development of a K-based intra-articular injection for OA treatment. Moreover, K performed significantly better than Na- or sucrose-based solutions, supporting the application of K toward improving irrigation solutions for joint surgery.

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Monocyte chemoattractant protein 1 induced chondrocytes degeneration and cartilage degradation in osteoarthritis

Cited by 6 publications

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Macrophage Activation in the Synovium of Healthy and Osteoarthritic Equine Joints

Macrophage Activation in the Synovium of Healthy and Osteoarthritic Equine Joints

Comparative analysis of macrophage activation in the synovium of healthy and osteoarthritic equine joints

Hyperosmolar Potassium (K⁺) Treatment Suppresses Osteoarthritic Chondrocyte Catabolic and Inflammatory Protein Production in a 3-Dimensional In Vitro Model

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Monocyte chemoattractant protein 1 induced chondrocytes degeneration and cartilage degradation in osteoarthritis

Cited by 6 publications

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Macrophage Activation in the Synovium of Healthy and Osteoarthritic Equine Joints

Macrophage Activation in the Synovium of Healthy and Osteoarthritic Equine Joints

Comparative analysis of macrophage activation in the synovium of healthy and osteoarthritic equine joints

Hyperosmolar Potassium (K+) Treatment Suppresses Osteoarthritic Chondrocyte Catabolic and Inflammatory Protein Production in a 3-Dimensional In Vitro Model

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Hyperosmolar Potassium (K⁺) Treatment Suppresses Osteoarthritic Chondrocyte Catabolic and Inflammatory Protein Production in a 3-Dimensional In Vitro Model