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Designing Biomaterials Surfaces to Direct Keratinocyte Functions at the Skin-Implant Interface

George Pins, Ph.D.

The implant-skin interface of percutaneous devices is generally weak and can fail when excessive loading disrupts the sealing of the interface by dermal and epidermal cells and tissue. As such, the formation of a stable implant-skin junction is a major factor in determining percutaneous implant success. In this study, we describe the use of functionalized self-assembled monolayers (SAMs) as a model system to assess the effects of biomaterial surface properties on controlling fibronectin (FN) conformation and concentration as well as keratinocyte function. By systematically analyzing FN adsorption at low and saturated surface densities, we distinguished between SAM-dependent effects of FN concentration and conformation on presenting cellular binding domains that direct cellular functions. Quantitative image analyses of immunostained samples showed that modulating the availability of the FN synergy site directly correlated with changes in keratinocyte attachment, spreading, and differentiation, through integrin-mediated signaling mechanisms. To further assess the functionality of these models, we have begun to characterize the mechanical adhesion of keratinocytes to these biomaterials surfaces as a function of fibronectin concentration. We anticipate that the results of these studies will be used to elucidate design features that can be incorporated into percutaneous implants to enhance the robustness of the skin-implant interface. Furthermore, these findings suggest that SAM-based model systems may be a valuable tool for designing and investigating the development of scaffolds that regulate the conformation of extracellular matrix cues and cellular functions that accelerate the rate of formation of the cutaneous seals around percutaneous devices.

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