Treatment with both TGF-β1 and PDGF-BB disrupts the stiffness-dependent myofibroblast differentiation of corneal keratocytes.

Unlabelled: During corneal wound healing, stromal keratocytes transform into a repair phenotype that is driven by the release of cytokines, like transforming growth factor-beta 1 (TGF-β1) and platelet-derived growth factor-BB (PDGF-BB). Previous work has shown that TGF-β1 promotes the myofibroblast differentiation of corneal keratocytes in a manner that depends on PDGF signaling. In addition, changes in mechanical properties are known to regulate the TGF-β1-mediated differentiation of cultured keratocytes.

Effects of Topography and PDGF on the Response of Corneal Keratocytes to Fibronectin-Coated Surfaces.

During corneal wound healing, corneal keratocytes are exposed to both biophysical and soluble cues that cause them to transform from a quiescent state to a repair phenotype. How keratocytes integrate these multiple cues simultaneously is not well understood. To investigate this process, primary rabbit corneal keratocytes were cultured on substrates patterned with aligned collagen fibrils and coated with adsorbed fibronectin.

Signaling Downstream of Focal Adhesions Regulates Stiffness-Dependent Differences in the TGF-1-Mediated Myofibroblast Differentiation of Corneal Keratocytes.

Following injury and refractive surgery, corneal wound healing can initiate a protracted fibrotic response that interferes with ocular function. This fibrosis is related, in part, to the myofibroblast differentiation of corneal keratocytes in response to transforming growth factor beta 1 (TGF-1). Previous studies have shown that changes in the mechanical properties of the extracellular matrix (ECM) can regulate this process, but the mechanotransductive pathways that govern stiffness-dependent changes in keratocyte differentiation remain unclear.

ECM stiffness modulates the proliferation but not the motility of primary corneal keratocytes in response to PDGF-BB.

During corneal wound healing, keratocytes present within the corneal stroma become activated into a repair phenotype upon the release of growth factors, such as transforming growth factor-beta 1 (TGF-β1) and platelet-derived growth factor-BB (PDGF-BB). The process of injury and repair can lead to changes in the mechanical properties of the tissue, and previous work has shown that the TGF-β1-mediated myofibroblast differentiation of corneal keratocytes depends on substratum stiffness. It is still unclear, however, if changes in stiffness can modulate keratocyte behavior in response to other growth factors, such as PDGF-BB.

ECM Stiffness Controls the Activation and Contractility of Corneal Keratocytes in Response to TGF-β1.

After surgery or traumatic injury, corneal wound healing can cause a scarring response that stiffens the tissue and impairs ocular function. This fibrosis is caused in part by the activation of corneal keratocytes from a native mechanically quiescent state to an activated myofibroblastic state. This transformation is tied to signaling downstream of transforming growth factor-β1 (TGF-β1).

Anisotropic, porous hydrogels templated by lyotropic chromonic liquid crystals.

Approaches to control the microstructure of hydrogels enable the control of cell-material interactions and the design of stimuli-responsive materials. We report a versatile approach for the synthesis of anisotropic polyacrylamide hydrogels using lyotropic chromonic liquid crystal (LCLC) templating. The orientational order of LCLCs in a mold can be patterned by controlling surface anchoring conditions, which in turn patterns the polymer network.