Increased expression of IL-6 family members in tendon pathology

Rheumatology (Oxford). 2012 Jul;51(7):1161-5. doi: 10.1093/rheumatology/kes002. Epub 2012 Feb 15.

Abstract

Objectives: Histological examination of pathological tendon generally does not reveal signs of inflammation. However, the inflammatory cytokine IL-6 has been shown to be expressed in ruptured rotator cuff tendon. The aim of this study was to investigate the expression of IL-6 family members in painful posterior tibialis tendon (PTT) and in painful and ruptured Achilles tendon (AT) compared with normal tendon.

Methods: AT samples were obtained from cadavers (normal) or from patients undergoing surgical procedures to treat chronic painful tendinopathy or ruptured tendon. PTT samples were obtained from patients undergoing surgery for other reasons (normal) and from patients with PTT dysfunction (painful). Total RNA was extracted and mRNA expression was analysed by quantitative real-time PCR.

Results: Collagen type I α-chain I (COL1A1) expression was increased in both painful PTT and AT compared with normal. Ciliary neurotrophic factor levels were increased in painful PTT only. In the painful AT, cyclooxygenase-2 (COX2) and IL-6 expression increased compared with normal. In the ruptured AT, levels of VEGF A, COX2, oncostatin-M, leukaemia inhibitory factor and IL-6 expression were higher compared with both normal and painful AT. IL-6R expression decreased in both painful and ruptured AT compared with normal.

Conclusion: Painful AT and PTT show different expression patterns, indicating a substantial difference between those two tendinopathies. Inflammatory markers are up-regulated in painful and particularly in ruptured AT, pointing towards a role of inflammation not only in rupture healing, but also in Achilles tendinopathy.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Achilles Tendon / injuries
  • Achilles Tendon / metabolism*
  • Achilles Tendon / pathology
  • Cadaver
  • Cells, Cultured
  • Chronic Disease
  • Ciliary Neurotrophic Factor / biosynthesis
  • Ciliary Neurotrophic Factor / genetics
  • Collagen Type I / biosynthesis
  • Collagen Type I / genetics
  • Cyclooxygenase 2 / biosynthesis
  • Cyclooxygenase 2 / genetics
  • Family
  • Female
  • Fibroblasts / metabolism
  • Fibroblasts / pathology
  • Gene Expression Regulation*
  • Humans
  • Immunohistochemistry
  • Interleukin-6 / biosynthesis
  • Interleukin-6 / genetics*
  • Male
  • Middle Aged
  • Posterior Tibial Tendon Dysfunction / etiology
  • Posterior Tibial Tendon Dysfunction / genetics*
  • Posterior Tibial Tendon Dysfunction / metabolism
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics*
  • Real-Time Polymerase Chain Reaction
  • Rupture
  • Severity of Illness Index
  • Tendinopathy / etiology
  • Tendinopathy / genetics*
  • Tendinopathy / metabolism
  • Tendon Injuries / complications
  • Tendon Injuries / genetics*
  • Tendon Injuries / metabolism
  • Vascular Endothelial Growth Factor A / biosynthesis
  • Vascular Endothelial Growth Factor A / genetics

Substances

  • Ciliary Neurotrophic Factor
  • Collagen Type I
  • Interleukin-6
  • RNA, Messenger
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • collagen type I, alpha 1 chain
  • Cyclooxygenase 2
  • PTGS2 protein, human