Ning Wang's blog

We demonstrate that a soft substrate of a stiffness that matches the embryonic stem cell stiffness can promote homogenous self-renewal and pluripotency of these cells, even in the absence of the growth factor-Leukemia Inhibitory Factor (LIF). These findings open the field of stem cell biology for long term culture of embryonic stem cells without generating a heterogeneous population of cells with varying degrees of differentiation and highlight the importance of mechanics in dictating embryonic stem cell pluripotency.

It is known that platelet derived growth factor (PDGF) induced Rac activation depends on Src activity. However, we find that a local stress of physiologic magnitude via integrins can directly activate Rac GTPase rapidly, independent of the Src activity. Our finding on the stress-induced rapid Rac activation challenges the conventional wisdom on mechanotransduction and suggests that stress-induced signaling via focal adhesions does not follow signal transduction pathways induced by growth factors. To view the whole paper:

We recently find that embryonic stem cells are very sensitive to a local cyclic stress applied to the focal adhesion.  They spread and differentiate (Oct3/4 downregulation) in response to this local force.

Over the last ten years, a peculiar behavior of living cells is revealed: their modulus increases weakly with loading frequency (the so-called weak power law behavior) (for a pure elastic solid, the slope is 0; for a viscous fluid, the slope is 1).  The underlying mechanism is not clear at all; although a phenomenological soft glass rheology model (a model based on a disordered structure system) has been proposed, it cannot explain the multi-power laws at different loading frequencies (see Stamenovic et al, Biophys J Letter, 2007). 

We recently find that podosomes, very dynamic, self-organized structures, can function as mechanosensors.  For details, see the recent issue of Current Biology.

It is generally believed that similar to soluble ligand-induced signal transduction, mechanotransduction initiates at the local force-membrane interface (e.g., at focal adhesions) by inducing local conformational changes or unfolding of membrane-bound proteins, followed by a cascade of diffusion-based or translocation-based signaling in the cytoplasm. However, all published reports, including past studies with the reporter type of construct extended here, were limited in timescale to address this fundamental issue.

What might be the differences, if there is any, between mechanical signaling and chemical signaling in a living cell?