Late matrix formation has been related to the ability of cells to rearrange the initially adsorbed protein layer, especially when comparing cell adhesion on hydrophilic and hydrophobic substrates [52] [54].
The dynamics of FN secretion and formation of a fibrillar matrix (late matrix) occurs preferentially on the samples with the higher contents of OH groups (Figure S5); see e.g. the 70%-OH SAM in Figure S5, where the presence of defined FN fibrils of higher fluorescence intensity can be observed.
These results support the hypothesis that late matrix formation is in need not only of cell adhesion on the substrate, but some cell movements, in the range of the size of the focal adhesion plaques, must take place so matrix deposition occurs normally [61].
As previously published, the resultant "late" matrices are reminiscent of in vivo desmoplastic ECMs which are characterized, among others, by a parallel patterned matrix fiber organization [ 44].
Nevertheless, in late matrices, beta-1 integrin inhibition prompted little effect in velocity, while cellular morphology, directionality, and relative track organization of the trajectories were greatly influenced.
SRL has evolved from the original model developed by Systems Development and Maturity Laboratory (SD&ML) at Stevens Institute of Technology to the latest Incidence Matrix SRL (IMSRL) model created from the doctoral research of London et al. at George Washington University [3, 4].
The grafts that hold the cells in place have evolved from periosteal flaps and collagen I/III covered membranes to the latest method, matrix-induced ACI (MACI) [19].
Late FN matrix formation was studied for longer times on the different SAMs (Figure S5).
This data suggests that, in the late-stage matrix, beta-1 integrin inhibition induces a change of invasive strategy.
We observed that beta1-integrin and/or PI3K pathways differentially regulate early vs. late stromal matrix induced (in vivo-like) invasive behavior.
