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Localized-plasmon voltammetry (LPV) bears great potential for electrochemical sensing applications beyond conventional cyclic voltammetry. In order to determine the limitations of this method, it is of utmost necessity to investigate the response toward chemical instability of the plasmonic electrode. We therefore investigated electrooxidation of a gold nanowire array with LPV in acidic electrolytes with different pH values. LPV shows excellent agreement with simultaneously recorded cyclic voltammograms up to the onset of oxygen evolution. Beyond that point, LPV still appears to provide meaningful signals. Further, with LPV the pH dependent reduction potentials of electrochemically grown gold oxides were determined and show a linear characteristic over the investigated pH range according to Nernst’s equation.

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Nanostructured substrates have been recognized to initiate transcriptional programs promoting cell proliferation. Specifically -catenin has been identified as transcriptional regulator, activated by adhesion to nanostructures. We set out to identify processes responsible for nanostructure-induced endothelial-catenin signaling. Transmission electron microscopy (TEM) of cell contacts to differently sized polyethylene terephthalate (PET) surface structures (ripples with 250 to 300 nm and walls with 1.5 μm periodicity) revealed different patterns of cell-substrate interactions. Cell adhesion to ripples occurred exclusively on ripple peaks, while cells were attached to walls continuously. The Src kinase inhibitor PP2 was active only in cells grown on ripples, while the Abl inhibitors dasatinib and imatinib suppressed -catenin translocation on both structures. Moreover, Gd sensitive Ca entry was observed in response to mechanical stimulation or Ca store depletion exclusively in cells grown on ripples. Both PP2 and Gd suppressed -catenin nuclear translocation along with proliferation in cells grown on ripples but not on walls. Our results suggest that adhesion of endothelial cells to ripple structured PET induces highly specific, interface topology-dependent changes in cellular signalling, characterized by promotion of Gd -sensitive Ca entry and Src/Abl activation. We propose that these signaling events are crucially involved in nanostructure-induced promotion of cell proliferation.

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