title: Increased expression of IL-6 family members in tendon pathology.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: School of Biological Sciences, University of East Anglia, Norwich Research Park, Norwich NR4 7TJ, UK. k.legerlotz@uea.ac.uk
authors.forename: Kirsten
authors.initials: K
authors.lastname: Legerlotz
authors.forename: Eleanor R
authors.initials: ER
authors.lastname: Jones
authors.forename: Hazel R C
authors.initials: HR
authors.lastname: Screen
authors.forename: Graham P
authors.initials: GP
authors.lastname: Riley
mesh_terms: D000125:Achilles Tendon / Q000293:injuries / Q000378:metabolism* / Q000473:pathology; D002102:Cadaver; D002478:Cells, Cultured; D002908:Chronic Disease; D020934:Ciliary Neurotrophic Factor / Q000096:biosynthesis / Q000235:genetics; D024042:Collagen Type I / Q000096:biosynthesis / Q000235:genetics; D000090602:Collagen Type I, alpha 1 Chain; D051546:Cyclooxygenase 2 / Q000096:biosynthesis / Q000235:genetics; D005190:Family; D005260:Female; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology; D005786:Gene Expression Regulation; D006801:Humans; D007150:Immunohistochemistry; D015850:Interleukin-6 / Q000096:biosynthesis / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D037081:Posterior Tibial Tendon Dysfunction / Q000209:etiology / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics*; D060888:Real-Time Polymerase Chain Reaction; D012421:Rupture; D012720:Severity of Illness Index; D052256:Tendinopathy / Q000209:etiology / Q000235:genetics* / Q000378:metabolism; D013708:Tendon Injuries / Q000150:complications / Q000235:genetics* / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis / Q000235:genetics
chemical_list: D020934:Ciliary Neurotrophic Factor; D024042:Collagen Type I; D000090602:Collagen Type I, alpha 1 Chain; D015850:Interleukin-6; D012333:RNA, Messenger; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human