Increased expression of IL-6 family members in tendon pathology

Legerlotz, Kirsten; Jones, Eldon M.; Screen, Hazel R. C.; Riley, Graham P.

doi:10.1093/rheumatology/kes002

Cited by 116 publications

(122 citation statements)

References 22 publications

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“…Interestingly, pro/antiinflammatory IL-6 expression showed no significant change by 2 d but significantly reduced by 1 wk after surgery with CTGF delivery. The temporal expression pattern of IL-6 by CTGF delivery, which is different from our in vitro outcome, is likely associated with the pro-and anti-inflammatory properties of IL-6 that are differently exhibited depending on healing phases and local inflammatory environment (41,42). Similar to IL-6, the CTGFinduced MMP-3 expression was different in between in vitro and in vivo tendon healing.…”

Section: Discussioncontrasting

confidence: 77%

Tendon stem/progenitor cells regulate inflammation in tendon healing via JNK and STAT3 signaling

et al. 2017

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Tendon stem/progenitor cells (TSCs) have been found in different anatomic locations and showed a promising regenerative potential. We identified a role of TSCs in the regulation of inflammation during healing of acute tendon injuries. Delivery of connective tissue growth factor (CTGF) into full-transected rat patellar tendons significantly increased the number of CD146 + TSCs, leading to enhanced healing. In parallel, CTGF delivery significantly reduced the number of iNOS + M1 macrophages and increased the expression of anti-inflammatory IL-10 at 2 d after surgery, with over 85%

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Section: Discussioncontrasting

confidence: 77%

Tendon stem/progenitor cells regulate inflammation in tendon healing via JNK and STAT3 signaling

et al. 2017

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“…Inflammatory genes, including VEGF, COX-2, IL-6, IL-6R and COL1A1, are upregulated in painful and particularly in ruptured Achilles tendons in humans [21]. Remarkably, our data showed that PRP had potential to downregulate COL1A1, VEGF, COX-2, IL-6, and IL-6R.…”

Section: Discussionsupporting

confidence: 49%

Platelet-rich Plasma Modulates the Secretion of Inflammatory/Angiogenic Proteins by Inflamed Tenocytes

Andı́a

Rubio‐Azpeitia

Maffulli

2015

Clinical Orthopaedics &Amp; Related Research

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Background Platelet-rich plasma therapies for tendinopathy appear to provide moderate pain reduction. However, the biological mechanisms behind the observed clinical effects remain poorly characterized. Questions/purposes The purpose of this study was to explore whether platelet-rich plasma modifies the inflammatory/angiogenic status of already inflamed tenocytes by examining (1) gene expression; (2) modulation of chemokine and interleukin secretion; and (3) differences between healthy and tendinopathic tenocytes. Methods Cells from both healthy and tendinopathic tendons were exposed to interleukin (IL)-1ß and after treated with platelet-rich plasma. Modifications in the expression of selected genes were assessed by real-time reverse transcription-polymerase chain reaction and changes in secretion of angiogenic/inflammatory molecules by enzyme-linked immunosorbent assay. Platelet-rich plasmainduced changes in tendinopathic cells were compared with normal after normalizing platelet-rich plasma data against IL-1ß status in each specific sample. Results In IL-1ß-exposed cells, platelet-rich plasma downregulates expression of IL-6/CXCL-6 (mean, 0.015; 95% confidence interval [CI], 0.005-0.025; p = 0.026), IL-6R (mean, 0.61; 95% CI, 0.27-0.95; p = 0.029), and IL-8/CXCL-8 (mean, 0.02; 95% CI, 0.007-0.023; p = 0.026). Secretion of IL-6/CXCL6, 0.35 (95% CI, 0.3-0.4; p = 0.002), IL-8/CXCL8, 0.55 (95% CI, 0.5-0.7; p = 0.01), and monocyte chemoattractant protein-1/CCL2, 0.40 (95% CI, 0.2-0.6; p = 0.001) was reduced by platelet-rich plasma, whereas vascular endothelial growth factor increased by twofold, (95% CI, 1.7-2.3; p \ 0.001). RANTES/CCL5 increased by10-fold (95% CI, 4-17) and hepatocyte growth factor by 21-fold (95% CI, 0.2-42) in tendinopathic and by 2.3-fold (95% CI, 2-3) and threefold (95% CI, 1-5) in normal cells (p = 0.005 for both). Conclusions Platelet-rich plasma induces an immunomodulatory and proangiogenic phenotype consistent with healing mechanisms with few differences between tendinopathic and normal cells. Clinical Relevance Platelet-rich plasma injections in pathological and nearby tissue might help to recover tendon homeostasis.

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“…We have previously shown that almost all MMP and ADAMTS enzymes are expressed in normal tendon, with different patterns of expression in normal, painful and ruptured tendon [36]. Although the pattern of metalloproteinase expression was similar in Achilles and posterior tibialis tendinopathy [36,52], there are differences in the expression of some genes that we speculate may be related to differences in mechanical loading [53].…”

Section: Introductionmentioning

confidence: 85%

Cyclical strain modulates metalloprotease and matrix gene expression in human tenocytes via activation of TGFβ

Jones

Legerlotz

et al. 2013

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Tendinopathies are a range of diseases characterised by degeneration and chronic tendon pain and represent a significant cause of morbidity. Relatively little is known about the underlying mechanisms; however onset is often associated with physical activity. A number of molecular changes have been documented in tendinopathy such as a decrease in overall collagen content, increased extracellular matrix turnover and protease activity. Metalloproteinases are involved in the homeostasis of the extracellular matrix and expression is regulated by mechanical strain. The aims of this study were to determine the effects of strain upon matrix turnover by measuring metalloproteinase and matrix gene expression and to elucidate the mechanism of action. Primary Human Achilles tenocytes were seeded in type I rat tail collagen gels in a Flexcell™ tissue train system and subjected to 5% cyclic uniaxial strain at 1 Hz for 48 h. TGFβ1 and TGFβRI inhibitor were added to selected cultures. RNA was measured using qRT-PCR and TGFβ protein levels were determined using a cell based luciferase assay. We observed that mechanical strain regulated the mRNA levels of multiple protease and matrix genes anabolically, and this regulation mirrored that seen with TGFβ stimulation alone. We have also demonstrated that the inhibition of the TGFβ signalling pathway abrogated the strain induced changes in mRNA and that TGFβ activation, rather than gene expression, was increased with mechanical strain. We concluded that TGFβ activation plays an important role in mechanotransduction. Targeting this pathway may have its place in the treatment of tendinopathy.

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Increased expression of IL-6 family members in tendon pathology

Cited by 116 publications

References 22 publications

Tendon stem/progenitor cells regulate inflammation in tendon healing via JNK and STAT3 signaling

Tendon stem/progenitor cells regulate inflammation in tendon healing via JNK and STAT3 signaling

Platelet-rich Plasma Modulates the Secretion of Inflammatory/Angiogenic Proteins by Inflamed Tenocytes

Cyclical strain modulates metalloprotease and matrix gene expression in human tenocytes via activation of TGFβ

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