Activation of stress-activated protein kinases (SAPK) in tendon cells following cyclic strain: the effects of strain frequency, strain magnitude, and cytosolic calcium.

摘要: Cyclic strain has been shown to benefit tendon health. However, repetitive loading also implicated in the etiology of overuse injuries. Recent studies demonstrated that several cell lines cyclic was associated with an activation stress-activated protein kinases (SAPKs). These SAPKs, turn, were be important upstream regulators a variety processes including apoptosis. To examine effect on SAPK cells vitro, canine patellar cyclically strained, and cellular stress response evaluated by measuring c-Jun N-terminal kinase (JNK) activation. The effects frequency magnitude as well role calcium signaling this mechanotransduction mechanism examined. resulted immediate JNK, which peaked at 30 min returned resting levels 2 h. This regulated magnitude-dependent but not frequency-dependent appeared mediated through calcium-dependent pathway. While transient JNK is normal processes, persistent linked initiation apoptotic cascade. A similar could responsible for initiating pathological events (localized death) seen injury.