We have evaluated
the response to nanotopography of CHO-K1 cells that express wild-type
paxillin or paxillin with mutations at serine 273 that inhibit phosphorylation.
Cells were grown on nanoporous and polished titanium surfaces. With
all cell types, immunofluorescence showed that adhesion and spreading
were minimally affected on the treated surface and that the actin
filaments were more abundant and well-aligned. Scanning electron microscopy
revealed changes in cell shape and abundant filopodia with lateral
nanoprotrusions in response to nanoporosity. Gene expression of proteins
associated with cellular adhesion and protrusions was significantly
increased on the nanoporous surface regardless of the cell type. In
particular, α-actinin, Rac1, Cdc42, and ITGα1 were upregulated
in S273 cells with alanine substitutions, whereas FAK, Pxn, and Src
were downregulated, leading to improved focal adhesion formation.
These findings suggest that the surface nanoporosity can “compensate
for” the genetic mutations that affect the biomechanical relationship
of cells to surfaces.