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Activation of stress‐activated protein kinases (SAPK) in tendon cells following cyclic strain: the effects of strain frequency, strain magnitude, and cytosolic calcium
Author(s) -
Arnoczky Steven P.,
Tian Tao,
Lavagnino Michael,
Gardner Keri,
Schuler Paul,
Morse Patrick
Publication year - 2002
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1016/s0736-0266(02)00038-4
Subject(s) - mechanotransduction , microbiology and biotechnology , kinase , strain (injury) , signal transduction , cytosol , apoptosis , biophysics , chemistry , cellular stress response , materials science , biology , biochemistry , anatomy , fight or flight response , enzyme , gene
Cyclic strain has been shown to benefit tendon health. However, repetitive loading has also been implicated in the etiology of tendon overuse injuries. Recent studies demonstrated that in several cell lines cyclic strain was associated with an activation of stress‐activated protein kinases (SAPKs). These SAPKs, in turn, were shown to be important upstream regulators of a variety of cell processes including apoptosis. To examine the effect of repetitive loading on SAPK activation in tendon cells in vitro, canine patellar tendon cells were cyclically strained, and the cellular stress response evaluated by measuring c‐Jun N‐terminal kinase (JNK) activation. The effects of strain frequency and strain magnitude as well as the role of calcium signaling in this mechanotransduction mechanism were also examined. Cyclic strain resulted in an immediate activation of JNK, which peaked at 30 min and returned to resting levels by 2 h. This activation was regulated by a magnitude‐dependent but not frequency‐dependent response and appeared to be mediated through a calcium‐dependent mechanotransduction pathway. While transient JNK activation is associated with normal cell processes, persistent JNK activation has been linked to the initiation of the apoptotic cascade. A similar mechanism could be responsible for initiating the pathological events (localized cell death) seen in tendon overuse injury. © 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved.