Durotaxis
Originally, this was believed to be an emergent metazoan property, as the phenomenon requires a complex sensory loop that is dependent on the communication of many different cells.
The first observations of durotaxis in isolated cells were that mechanical stimuli could cause the initiation and elongation of axons in the sensory and brain neurons of chicks and induce motility in previously stationary fish epidermal keratocytes.
Elastin - as its name suggests - is a highly elastic protein with an important role in tissues that need to return to their original positions after deformation, such as skin, blood vessels, and lungs.
[15][16] In biological research, the rigidity (or stiffness) is commonly measured using Young's modulus of elasticity, the ratio of stress to strain along an axis, in Pascals.
These methods induce distortion in the tissue and measure the mechanical properties, usually with ultrasound or magnetic resonance imaging (MRI).
[29] Cell signaling is a product of both the physical and biochemical properties of the ECM and interaction between these two pathways is crucial to understand cellular responses.
For example, bone morphogenetic protein (BMP) - a growth factor - is unable to induce osteogenesis under insufficient cytoskeletal tension.
Increased external stiffness leads to a signal transduction cascade that activates the small GTPase Rho and Rho-associated kinase (ROCK).
The stronger mechanical feedback would pull the cell towards the stiffer region and cause a bias in directional movement and have other consequences on cytoskeletal and focal adhesion organization.
[11] Consequently, durotaxis must rely on continuous sampling of ECM stiffness over space and time in a process called rigidity mechanosensing.
[32] Recent research has revealed that individual focal adhesions do not necessarily exert stable traction forces in response to unchanging ECM stiffness.
High-resolution TFM allows the analysis of traction forces at much smaller structures, such as focal adhesions, at a spatial resolution of ≈1 μm.
Experiments in mice have demonstrated that tumor cells preferentially invade into the adjacent stroma along stiff collagen fibers.
[40] Increased liver stiffness (of existing collagen) has actually been shown to precede fibrosis and to be required for the activation of fibrogenic myofibroblasts.
The pathology of atherosclerosis is largely dependent on the migration of vascular smooth muscle cells (VSMCs) into the tunica intima layer of the blood vessel, where they can accumulate lipids, undergo necrosis, and elaborate the ECM (fibrosis).
