Cytokines and apoptosis in supraspinatus tendinopathy.

@article{Millar2009CytokinesAA,
  title={Cytokines and apoptosis in supraspinatus tendinopathy.},
  author={Neal L. Millar and Aiqun Wei and Timothy J. Molloy and Fiona Bonar and George A.C. Murrell},
  journal={The Journal of bone and joint surgery. British volume},
  year={2009},
  volume={91 3},
  pages={
          417-24
        }
}
  • N. Millar, A. Wei, +2 authors G. Murrell
  • Published 1 March 2009
  • Biology, Medicine
  • The Journal of bone and joint surgery. British volume
The role of inflammatory cells and their products in tendinopathy is not completely understood. Pro-inflammatory cytokines are upregulated after oxidative and other forms of stress. Based on observations that increased cytokine expression has been demonstrated in cyclically-loaded tendon cells we hypothesised that because of their role in oxidative stress and apoptosis, pro-inflammatory cytokines may be present in rodent and human models of tendinopathy. A rat supraspinatus tendinopathy model… 
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IL-17A mediates inflammatory and tissue remodelling events in early human tendinopathy
TLDR
IL-17A is proposed as an inflammatory mediator within the early tendinopathy processes thus providing novel therapeutic approaches in the management of tendon disorders.
Hypoxia: a critical regulator of early human tendinopathy
TLDR
Hypoxia promotes the expression of proinflammatory cytokines, key apoptotic mediators and drives matrix component synthesis towards a collagen type III profile by human tenocytes.
Inflammation is Present in Early Human Tendinopathy
TLDR
Evidence is provided for an inflammatory cell infiltrate in early mild/moderate human tendinopathy, and significant infiltration of mast cells and macrophages is demonstrated, suggesting a role for innate immune pathways in the events that mediate early tend inopathy.
Targeting danger molecules in tendinopathy: the HMGB1/TLR4 axis
TLDR
HMGB1 is proposed as a mediator driving the inflammatory/matrix crosstalk and manipulation of the HMGB1/TLR4 axis may offer novel therapeutic approaches targeting inflammatory mechanisms in the management of human tendon disorders.
Mast cells exert pro-inflammatory effects of relevance to the pathophyisology of tendinopathy
TLDR
It is demonstrated that mast cell-derived PGE2 reduces collagen synthesis and enhances expression and activities of MMPs in human tenocytes.
Increased levels of apoptosis and p53 in partial-thickness supraspinatus tendon tears
TLDR
Higher density of apoptotic tendon cells and the density of cells expressing p53 were significantly increased in both the partially torn supraspinatus tendons and in the matched subscapularis tendons, compared with uninjured reference tendons.
INCREASED LEVELS OF APOPTOSIS AND P53 IN PARTIAL-THICKNESS SUPRASPINATUS TENDON TEARS
TLDR
The presence of increased apoptosis and p53 in partial-thickness tears of the supraspinatus tendon is accompanied by features of both degeneration as well as ongoing repair.
Persistent stromal fibroblast activation is present in chronic tendinopathy
TLDR
Stromal fibroblast activation markers are increased and persist in diseased compared to healthy tendon tissues and cells, and may be implicated in the development of chronic inflammation and recurrent tendinopathy.
Local biochemical and morphological differences in human Achilles tendinopathy: a case control study
TLDR
The present data supports the notion that tendinopathy is an ongoing degenerative process as no fibrillogenesis, inflammation or wound healing could be detected, and an increased expression of factors stimulating the turnover of connective tissue is present in the diseased part of tendinopathic tendons.
Tenocyte apoptosis in the torn rotator cuff: a primary or secondary pathological event?
TLDR
The results suggest that tenocyte apoptosis results from more than one mechanism in the injured rotator cuff, including both intrinsic factors related specifically to the torn supraspinatus tendon, as well as a more generalised effect on the adjacent subscapularis tendon.
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References

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