IL-10 overexpression differentially affects cartilage matrix gene expression in response to TNF-α in human articular chondrocytes in vitro

Is resection of the tendon edge necessary to enhance the healing process? An evaluation of the expression of collagen type I, IL-1β, IFN-γ, IL-4, and IL-13 in the distal 1 cm of a torn supraspinatus tendon: part II

“…The findings of part I 17 and part II of the study, together with the current knowledge concerning the influence of molecular factors on inflammatory and apoptotic processes, 1,2,12,[24][25][26]36,38,40 confirm the growing need for a proper understanding of their influence on rotator cuff healing. They demonstrate the need for further research on both these factors and the pharmacologic support that can be provided in the near future.…”

“…26,38 As apoptosis is connected with a fall in tenocyte number in the affected area, 5,32,49 the potential for collagen production is thus reduced, which may additionally impair the action of IFNg to slow their prolifieration. 1 The ability of tenocytes to produce collagen is manifested in an observed rise of type I collagen expression 43 (Tables I and II) in the proximal direction.…”

Carboxymethyl‑chitosan attenuates inducible nitric oxide synthase and promotes interleukin‑10 production in rat chondrocytes

“…This downregulation of IL-10 was associated with a reduction in T cell immunoglobulin mucin receptor 3 expres-T cell immunoglobulin mucin receptor 3 expres-expression (39). In human articular chondrocytes IL-10 may upregulate the expression of type II collagen and promote cartilage-specific extracellular matrix synthesis in response to TNF-α (40). In the present study, the results suggested that IL-10 activation was correlated with inhibition of iNOS production and was associated with the protective role of CM-chitosan against OA.…”

Molecular Effects of Exercise in Rheumatoid Arthritis

“…IL-10 treatment in an antigen-induced arthritis animal model resulted in a marked reduction of TNF-levels (Lubberts et al 1998). In human chondrocytes treated with TNF-, IL-10 overexpression ssuppressed MMP-13 levels and antagonized the TNF--mediated suppression of aggrecan (Muller et al 2008). It has been hypothesized that IL-10 may exert its effects by stimulating the production of endogenous TNF-inhibitors such as soluble TNF-receptors (Fernandes et al 2002).…”