No inflammatory gene-expression response to acute exercise in human Achilles tendinopathy
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No inflammatory gene-expression response to acute exercise in human Achilles tendinopathy. / Pingel, Jessica; Fredberg, Ulrich; Mikkelsen, Lone Ramer; Schjerling, Peter; Heinemeier, Katja Maria; Kjær, Michael; Harrison, Adrian Paul; Langberg, Henning.
In: European Journal of Applied Physiology, Vol. 113, No. 8, 2013, p. 2101-2109.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - No inflammatory gene-expression response to acute exercise in human Achilles tendinopathy
AU - Pingel, Jessica
AU - Fredberg, Ulrich
AU - Mikkelsen, Lone Ramer
AU - Schjerling, Peter
AU - Heinemeier, Katja Maria
AU - Kjær, Michael
AU - Harrison, Adrian Paul
AU - Langberg, Henning
N1 - CURIS 2013 NEXS 181
PY - 2013
Y1 - 2013
N2 - Although histology data favour the view of a degenerative nature of tendinopathy, indirect support for inflammatory reactions to loading in affected tendons exists. The purpose of the present study was to elucidate whether inflammatory signalling responses after acute mechanical loading were more pronounced in tendinopathic versus healthy regions of human tendon and if treatment with non-steroidal anti-inflammatory medications (NSAID's) reduces this response. Twenty-seven tendinopathy patients (>6 months) were randomly assigned to a placebo (n = 14) or NSAID (Ibumetin NYCOMED GmbH Plant Oranienburg Germany (600 mg) × 3/day/1 week) group (n = 13) in a double-blinded-fashion. Tendon biopsies were taken from the painful and a healthy region of the same tendon 2 h after 1 h running. Gene-expression of several targets was analysed in the sampled Achilles tendon biopsies. The mRNA for TGF-ß, collagen-I and collagen-III were significantly higher expressed, and decorin, CTGF, IL-6 and IL-10 were significantly lower expressed in the tendinopathic versus healthy tendon area. Only IL-10 was lower in expression in experiments with NSAID administration, while all other determined parameters were unaffected by NSAID. All ultrasonographic outcomes were unchanged in response to acute exercise and not influenced by NSAID. The signalling for collagen and TGF-beta was upregulated after acute loading in tendinopathic tendon. In contrast to the hypothesis, inflammatory signalling was not exaggerated in tendinopathic tendon 2 h after acute mechanical loading.
AB - Although histology data favour the view of a degenerative nature of tendinopathy, indirect support for inflammatory reactions to loading in affected tendons exists. The purpose of the present study was to elucidate whether inflammatory signalling responses after acute mechanical loading were more pronounced in tendinopathic versus healthy regions of human tendon and if treatment with non-steroidal anti-inflammatory medications (NSAID's) reduces this response. Twenty-seven tendinopathy patients (>6 months) were randomly assigned to a placebo (n = 14) or NSAID (Ibumetin NYCOMED GmbH Plant Oranienburg Germany (600 mg) × 3/day/1 week) group (n = 13) in a double-blinded-fashion. Tendon biopsies were taken from the painful and a healthy region of the same tendon 2 h after 1 h running. Gene-expression of several targets was analysed in the sampled Achilles tendon biopsies. The mRNA for TGF-ß, collagen-I and collagen-III were significantly higher expressed, and decorin, CTGF, IL-6 and IL-10 were significantly lower expressed in the tendinopathic versus healthy tendon area. Only IL-10 was lower in expression in experiments with NSAID administration, while all other determined parameters were unaffected by NSAID. All ultrasonographic outcomes were unchanged in response to acute exercise and not influenced by NSAID. The signalling for collagen and TGF-beta was upregulated after acute loading in tendinopathic tendon. In contrast to the hypothesis, inflammatory signalling was not exaggerated in tendinopathic tendon 2 h after acute mechanical loading.
U2 - 10.1007/s00421-013-2638-3
DO - 10.1007/s00421-013-2638-3
M3 - Journal article
C2 - 23588255
VL - 113
SP - 2101
EP - 2109
JO - European Journal of Applied Physiology
JF - European Journal of Applied Physiology
SN - 1439-6319
IS - 8
ER -
ID: 45258288