Bone is known for its ability to self-repair the microdamage and actively adapt to its mechanical environment, both of which are under the coordination of bone cells. Mechanical cues are sensed by cells and converted into cellular events in a process called mechanotransduction [1]. Most theories of mechanotransduction are based on direct stimulus of cell surface receptors by substrate deformation, fluid shear and/or hydrostatic pressure [2]. Yet, mechanical stimulus may come to affect cell response indirectly, via pathways which alter the pericellular niche. Such indirect pathways of mechanotransduction are not well-investigated for bone.

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