Interleukin-1? Increases Elasticity of Human Bioartificial Tendons

Qi, Jie; Chi, Liqun; Maloney, Melissa; Yang, Xi; Bynum, Donald K.; Banes, Albert J.

doi:10.1089/ten.2006.12.ft-228

Cited by 4 publications

(12 citation statements)

References 53 publications

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“…Expression of the main extracellular matrix component in tendon, type I collagen was downregulated by TNFα. This corresponds with the results of Pan and Halper,23 and a reduction of the type I collagen expression was also shown for another prototype pro‐inflammatory cytokine, IL‐1β 24, 25. The disintegration of extracellular matrix components is carried out by matrix degrading enzymes such as MMPs.…”

Section: Discussionsupporting

confidence: 88%

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Effect of pro‐inflammatory and immunoregulatory cytokines on human tenocytes

John

Lodka

Kohl

et al. 2010

Journal Orthopaedic Research

134

104

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Tendon injury induces a local inflammatory response, characterized by the induction of pro-inflammatory cytokines. The aim of the present study was to analyze the effects of TNFa, IL-6 and IL-10 on key parameters of tendon homeostasis. Cultured primary human tenocytes were treated with the recombinant cytokines IL-6, IL-10, TNFa, or combinations of TNFa with IL-6 and IL-10 (10 ng/mL, 6, 24 h). Expression of type I collagen, elastin, MMP-1, TNFa, IL-1b, IL-6, IL-10, and suppressors of cytokine signaling (SOCS1, 3) was analyzed with the use of RTD-PCR, immunocytochemistry, and Western blot analysis. In response to TNFa, tenocytes reduced their type I collagen deposition but increased their elastin gene expression and highly upregulated their expression for MMP-1, pro-inflammatory (TNFa, IL-1b) and immunoregulatory (IL-6, IL-10) cytokines. TNFa stimulation augmented SOCS1, whereas SOCS3 expression in tenocytes was also induced by IL-6. The treatment of tenocytes with IL-6 and IL-10 had no effect on cytokine expression. Neither IL-6 nor IL-10 modulated the observed effects of TNFa significantly. These results indicate that TNFa strongly activates the tenocytes to amplify their own TNFa expression and, subsequently, that of other regulatory cytokines and matrix degrading enzymes. However, the impact of IL-6 and IL-10 on tenocytes remains unclear. ß

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Section: Discussionsupporting

confidence: 88%

“…In contrast to this catabolic effect on extracellular tendon matrix, the elastin expression was significantly induced by TNFα. Qi et al reported a similar stimulation of the elastin gene expression by the pro‐inflammatory cytokine IL‐1β 24. This indicates that there exist distinct anabolic effects of TNFα.…”

Section: Discussionmentioning

confidence: 85%

Effect of pro‐inflammatory and immunoregulatory cytokines on human tenocytes

John

Lodka

Kohl

et al. 2010

Journal Orthopaedic Research

134

104

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“…In contrast, type I collagen is mainly responsible for tendon stiffness. Obviously, both components (type I collagen and elastin) are differently regulated in tendon by cytokines (Qi et al, 2006a; John et al, 2010). While collagen provides the tissue with its tensile strength, proteoglycans play a role in tissue hydration and regulate collagen integrity (Rees et al, 2009).…”

Section: Tendon Organizationmentioning

confidence: 99%

“…While collagen provides the tissue with its tensile strength, proteoglycans play a role in tissue hydration and regulate collagen integrity (Rees et al, 2009). It is well known that deposition and expression of ECM components such as collagens and proteoglycans can be regulated by pro‐inflammatory cytokines in connective tissue cells (Seguin et al, 2005; Qi et al, 2006a; Thampatty et al, 2007; John et al, 2010). In tendon disorders such as tendopathy as well as post tendon injury, a shift of the proteoglycan deposition has been observed (Lo et al, 2005; Rees et al, 2009; Samiric et al, 2009; Lui et al, 2010).…”

Section: Tendon Organizationmentioning

confidence: 99%

“…Interestingly, Tohyama et al (2007) reported that extrinsic fibroblasts that immigrate from outside into the healing tissue were less sensitive to pro‐inflammatory cytokines such as IL‐1β compared with tenocytes. These cytokines suppressed ECM synthesis such as that of type I collagen (Qi et al, 2006a; John et al, 2010). However, the expression of other ECM components such as elastin was up‐regulated by TNFα (John et al, 2010).…”

Section: Role Of Il‐1β and Tnfα In Tendon And Tenocytesmentioning

confidence: 99%

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The role of pro‐inflammatory and immunoregulatory cytokines in tendon healing and rupture: new insights

Schulze‐Tanzil

Al-Sadi

Wiegand

et al. 2011

Scandinavian Med Sci Sports

138

117

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Owing to limited self-healing capacity, tendon ruptures and healing remain major orthopedic challenges. Increasing evidence suggests that post-traumatic inflammatory responses, and hence, cytokines are involved in both cases, and also in tendon exercise and homeostasis. This review summarizes interrelations known between the cytokines interleukin (IL)-1β, tumor necrosis factor (TNF)α, IL-6 and vascular endothelial growth factor (VEGF) in tendon to assess their role in tendon damage and healing. Exogenic cytokine sources are blood-derived leukocytes that immigrate in damaged tendon. Endogenous expression of IL-1β, TNFα, IL-6, IL-10 and VEGF was demonstrated in tendon-derived cells. As tendon is a highly mechanosensitive tissue, cytokine homeostasis and cell survival underlie an intimate balance between adequate biomechanical stimuli and disturbance through load deprivation and overload. Multiple interrelations between cytokines and tendon extracellular matrix (ECM) synthesis, catabolic mediators e.g. matrix-degrading enzymes, inflammatory and angiogenic factors (COX-2, PGE2, VEGF, NO) and cytoskeleton assembly are evident. Pro-inflammatory cytokines affect ECM homeostasis, accelerate remodeling, amplify biomechanical adaptiveness and promote tenocyte apoptosis. This multifaceted interplay might both contribute to and interfere with healing. Much work must be undertaken to understand the particular interrelation of these inflammatory and regulatory mediators in ruptured tendon and healing, which has relevance for the development of novel immunoregulatory therapeutic strategies.

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Species variations in tenocytes’ response to inflammation require careful selection of animal models for tendon research

Oreff

Fenu

Vogl

et al. 2021

Preprint

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For research on tendon injury, many different animal models are utilized; however, the extent to which these species simulate the clinical condition and disease pathophysiology has not yet been critically evaluated. Considering the importance of inflammation in tendon disease, this study compared the cellular and molecular features of inflammation in tenocytes of humans and four common model species (mouse, rat, sheep, and horse). While mouse and rat tenocytes most closely equalled human tenocytes low proliferation capacity and the negligible effect of inflammation on proliferation, the wound closure speed of humans was best approximated by rats and horses. The overall gene expression of human tenocytes was most similar to mice under healthy, to horses under transient and to sheep under constant inflammatory conditions. Humans were best matched by mice and horses in their tendon marker and collagen expression, by horses in extracellular matrix remodelling genes, and by rats in inflammatory mediators. As no single animal model perfectly replicates the clinical condition and sufficiently emulates human tenocytes, fit-for-purpose selection of the model species for each specific research question and combination of data from multiple species will be essential to optimize translational predictive validity.

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Interleukin-1? Increases Elasticity of Human Bioartificial Tendons

Cited by 4 publications

References 53 publications

Effect of pro‐inflammatory and immunoregulatory cytokines on human tenocytes

Effect of pro‐inflammatory and immunoregulatory cytokines on human tenocytes

The role of pro‐inflammatory and immunoregulatory cytokines in tendon healing and rupture: new insights

Species variations in tenocytes’ response to inflammation require careful selection of animal models for tendon research

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