Interleukin-10 modulates pro-apoptotic effects of TNF-α in human articular chondrocytes in vitro

John, Thilo; Müller, R. D.; Oberholzer, Andreas; Zreiqat, Hala; Kohl, Benjamin; Ertel, Wolfgang; Hostmann, Arwed; Tschoeke, Sven K.; Schulze‐Tanzil, Gundula

doi:10.1016/j.cyto.2007.10.002

Cited by 80 publications

(79 citation statements)

References 46 publications

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“…The role of IL-18 on regulating apoptosis is controversial and seems to be driven by cell type-specific mechanisms. IL-18 inhibits neutrophil apoptosis (19) while it accelerates cell death in chondrocytes (22) and renal tubular cells (54). Secondly, we found that immobilized IL-18 stimulates macrophage adhesion to fibrinogen in a Mac-1-dependent fashion.…”

Section: Discussionmentioning

confidence: 71%

Macrophage-derived IL-18 and increased fibrinogen deposition are age-related inflammatory signatures of vascular remodeling

Rodriguez-Menocal

Faridi

Martinez

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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Padron RI. Macrophage-derived IL-18 and increased fibrinogen deposition are age-related inflammatory signatures of vascular remodeling. Am J Physiol Heart Circ Physiol 306: H641-H653, 2014. First published January 10, 2014; doi:10.1152/ajpheart.00641.2013.-Aging has been associated with pathological vascular remodeling and increased neointimal hyperplasia. The understanding of how aging exacerbates this process is fundamental to prevent cardiovascular complications in the elderly. This study proposes a mechanism by which aging sustains leukocyte adhesion, vascular inflammation, and increased neointimal thickness after injury. The effect of aging on vascular remodeling was assessed in the rat balloon injury model using microarray analysis, immunohistochemistry, and LINCOplex assays. The injured arteries in aging rats developed thicker neointimas than those in younger animals, and this significantly correlated with a higher number of tissue macrophages and increased vascular IL-18. Indeed, IL-18 was 23-fold more abundant in the injured vasculature of aged animals compared with young rats, while circulating levels were similar in both groups of animals. The depletion of macrophages in aged rats with clodronate liposomes ameliorated vascular accumulation of IL-18 and significantly decreased neointimal formation. IL-18 was found to inhibit apoptosis of vascular smooth muscle cells (VSMC) and macrophages, thus favoring both the formation and inflammation of the neointima. In addition, injured arteries of aged rats accumulated 18-fold more fibrinogen-␥ than those of young animals. Incubation of rat peritoneal macrophages with immobilized IL-18 increased leukocyte adhesion to fibrinogen and suggested a proinflammatory positive feedback loop among macrophages, VSMC, and the deposition of fibrinogen during neointimal hyperplasia. In conclusion, our data reveal that concentration changes in vascular cytokine and fibrinogen following injury in aging rats contribute to local inflammation and postinjury neointima formation. inflammation; vascular injury; aging; neointima; vascular smooth muscle cells AGING IS RECOGNIZED AS A MAJOR and independent risk factor for the development of vascular restenosis (29). This risk can be explained by profound, age-dependent changes in vascular structure and physiology that lead to endothelial dysfunction (18) and a chronic inflammatory stage (53), which impair healing and render a vascular system prone to develop occlusive neointimas in response to injury. However, even when this notion is largely accepted, the mechanisms by which aging alters vascular physiology and repair have remained understudied to date.The process of aging increases and sustains inflammation within the vascular wall (52). Macrophages are commonly recognized as the most important cell type in the chronicity of this process (37). Indeed, inflammation in arteries of aged individuals is evidenced by an excessive accumulation of macrophages in the inner layer of the arterial wall (intima), and this occurs in the presence o...

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Section: Discussionmentioning

confidence: 71%

Macrophage-derived IL-18 and increased fibrinogen deposition are age-related inflammatory signatures of vascular remodeling

Rodriguez-Menocal

Faridi

Martinez

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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“…However, this is the first work to present the capacity of human supraspinatus tenocytes to prevent both the apoptotic and inflammatory processes by the increased expression of antiapoptotic Bcl-2, 26 and antiinflammatory IL-10 molecules. 20 Research by Millar et al 27 confirms that the tenocytes of the torn supraspinatus tendon have the capacity to produce TNF-a and also notes a positive correlation between TNF-a expression and caspase 8 concentration. The TNF-a cytokine is associated with the capacity to stimulate tenocyte apoptosis.…”

Section: Discussionmentioning

confidence: 79%

Is resection of the tendon edge necessary to enhance the healing process? An evaluation of the homeostasis of apoptotic and inflammatory processes in the distal 1 cm of a torn supraspinatus tendon: part I

Fabiś¹,

Szemraj²,

Strek³

et al. 2014

Journal of Shoulder and Elbow Surgery

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“…MV treatment determined a significant IL-10 enhancement compared with EX, which may be related to its content of annexin A1 [36]. The increased production of IL-10 may then contribute to the anti-inflammatory effects of CM and its EV as this cytokine inhibits the synthesis of pro-inflammatory cytokines [37] and antagonizes their deleterious effects on chondrocyte metabolism [38, 39]. …”

Section: Discussionmentioning

confidence: 99%

Microvesicles from Human Adipose Tissue-Derived Mesenchymal Stem Cells as a New Protective Strategy in Osteoarthritic Chondrocytes

Tofiño-Vian

Guillén

Caz

et al. 2018

Cell Physiol Biochem

182

141

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Background/Aims: Chronic inflammation contributes to cartilage degeneration during the progression of osteoarthritis (OA). Adipose tissue-derived mesenchymal stem cells (AD-MSC) show great potential to treat inflammatory and degradative processes in OA and have demonstrated paracrine effects in chondrocytes. In the present work, we have isolated and characterized the extracellular vesicles from human AD-MSC to investigate their role in the chondroprotective actions of these cells. Methods: AD-MSC were isolated by collagenase treatment from adipose tissue from healthy individuals subjected to abdominal lipectomy surgery. Microvesicles and exosomes were obtained from conditioned medium by filtration and differential centrifugation. Chondrocytes from OA patients were used in primary culture and stimulated with 10 ng/ml interleukin(IL)-1β in the presence or absence of AD-MSC microvesicles, exosomes or conditioned medium. Protein expression was investigated by ELISA and immunofluorescence, transcription factor-DNA binding by ELISA, gene expression by real-time PCR, prostaglandin E₂ (PGE₂) by radioimmunoassay, and matrix metalloproteinase (MMP) activity and nitric oxide (NO) production by fluorometry. Results: In OA chondrocytes stimulated with IL-1β, microvesicles and exosomes reduced the production of inflammatory mediators tumor necrosis factor-α, IL-6, PGE₂ and NO. The downregulation of cyclooxygenase-2 and microsomal prostaglandin E synthase-1 would lead to the decreased PGE₂ production while the effect on NO could depend on the reduction of inducible nitric oxide synthase expression. Treatment of OA chondrocytes with extracellular vesicles also decreased the release of MMP activity and MMP-13 expression whereas the production of the anti-inflammatory cytokine IL-10 and the expression of collagen II were significantly enhanced. The reduction of inflammatory and catabolic mediators could be the consequence of a lower activation of nuclear factor-κB and activator protein-1. The upregulation of annexin A1 specially in MV may contribute to the anti-inflammatory and chondroprotective effects of AD-MSC. Conclusions: Our data support the interest of AD-MSC extracellular vesicles to develop new therapeutic approaches in joint conditions.

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Interleukin-10 modulates pro-apoptotic effects of TNF-α in human articular chondrocytes in vitro

Cited by 80 publications

References 46 publications

Macrophage-derived IL-18 and increased fibrinogen deposition are age-related inflammatory signatures of vascular remodeling

Macrophage-derived IL-18 and increased fibrinogen deposition are age-related inflammatory signatures of vascular remodeling

Is resection of the tendon edge necessary to enhance the healing process? An evaluation of the homeostasis of apoptotic and inflammatory processes in the distal 1 cm of a torn supraspinatus tendon: part I

Microvesicles from Human Adipose Tissue-Derived Mesenchymal Stem Cells as a New Protective Strategy in Osteoarthritic Chondrocytes

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