Introduction

Large-scale mechanical forces due to gravity, movement, air flow, and hemodynamic forces have been recognized to be important regulators of tissue form and function for more than a century. The effects of compression on bone, tension on muscle, respiratory motion on lung, and shear on blood vessels are a few prime examples. Although interest in mechanics waned when biology shifted its focus to chemicals and genes in the middle of the last century, there has been a recent renaissance in the field of mechanical biology. Physical forces are now known to be key regulators of virtually all facets of molecular and cellular behavior, as well as developmental control and wound repair [1]. Impaired mechanical signaling also underlies many diseases, and numerous clinical therapies utilize mechanical stimulation to produce their healing effects [2]. However, we still do not fully understand “mechanotransduction” – the process by which individual cells sense and respond to mechanical forces by altering biochemistry and gene expression.

To understand how individual cells respond to mechanical forces, we need to define how stresses are borne and distributed within cells, as well as how they are focused on critical molecular elements that mediate mechanochemical conversion. Early studies assumed that mechanotransduction might be mediated through generalized deformation of the cell’s surface membrane that produced changes in membrane-associated signal transduction. Although this may occur, it is now clear that multiple molecules and structures distributed throughout the membrane, cytoplasm, cytoskeleton, and nucleus contribute to the mechanotransduction response that governs cell behavioral control [1, 3, 4]. Thus, it is critical that we understand how cells are structured so that mechanical stresses are channeled and focused simultaneously on the various key conversion molecules and structures that mediate the transduction response.