抄録
Depletion of nesprin-1, a component of the linker of nucleoskeleton and cytoskeleton (LINC) complex mediating mechanical interactions between cytoskeletons and the nucleus, cause abolishment of cellular morphological changes in response to mechanical stimuli. This suggests that bindings of the nucleus to actin filaments through nesprin-1 play and important role in cell morphological responses to mechanical environments. In the present study, to further reveal the role of the actin filament-nucleus interaction, morphological changes of nesprin-1 depleted fibroblasts exposed to cyclic stretching were investigated. Fibroblasts treated with siRNA against nesprin-1 were exposed to cyclic stretching at 1 Hz for 24 h. Non-treated cell exhibited more elongated shapes and oriented perpendicular to the direction of stretching after exposure. siRNA-treated cells showed orientation in response to cyclic stretching but did not elongate and exhibited similar shapes to those of statically cultured cells. These results indicate that nesprin-1 depletion causes suppression of cell elongation in response to mechanical stimuli.
