Various cell types can sense and convert mechanical forces into biochemical signaling events through a process called mechanotransduction, and this process is often highly specific to the types of mechanical forces applied. However, the mechanism(s) that allow for specificity in mechanotransduction remain undefined. Thus, the goal of this study was to gain insight into how cells distinguish among specific types of mechanical information. To accomplish this goal, we determined if skeletal myoblasts can distinguish among differences in strain, strain rate, and strain-time integral (STI). Our results demonstrate that mechanically induced signaling through the c-jun N-terminal kinase 2 [JNK2] is elicited via a mechanism that depends on an interaction between the magnitude of strain and strain rate and is independent of STI. In contrast to JNK2, mechanically induced signaling through the ribosomal S6 kinase [p70(389)] is not strain rate sensitive, but instead involves a magnitude of strain and STI dependent mechanisms. Mathematical modeling also indicated that mechanically induced signaling through JNK2 and p70(389) can be isolated to separate viscous and elastic mechanosensory elements, respectively. Based on these results, we propose that skeletal myoblasts contain multiple mechanosensory elements with distinct biomechanical properties and that these distinct biomechanical properties provide a mechanism for specificity in mechanotransduction.
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