RhoA Controls Wnt Upregulation on Microstructured Titanium Surfaces

Figure 5

Diagram depicting the proposed model for RhoA role in cell responses to substrate topography. Noncanonical Wnt factors bind to receptor dimers Frizzled-Ror2C, which activate RhoA. Rho, in turns, activates downstream target Myosin Light Chain Kinase (MLCK), which phosphorylates Myosin II. Acto-Myosin filaments create cell tension, which facilitates the activation of canonical Wnt signaling and promotes b catenin release from its destruction complex and translocation to the nucleus possibly by acting on tension sensitive structures (focal adhesions). A feedback loop from tension-activated structures controls RhoA activation levels. Actin microfilaments can control RhoA too, as their partial disruption increases RhoA activity and canonical Wnt activation.