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. Author manuscript; available in PMC: 2018 Jan 1.
Published in final edited form as: Biomaterials. 2016 Nov 16;115:155–166. doi: 10.1016/j.biomaterials.2016.11.019

Figure 3. Topographical variation promotes endothelial cell migration and proliferation through disruption of VE-cadherin junctions.

Figure 3

a) Motility track plots of ECs cultured on ELP fabrics with varied fiber widths, with and without VE-cadherin blocking antibody (15 representative tracks per condition shown; 600 cells tracked for 16 hours per condition). b) Average motility speed quantified from tracks. ECs migrated at a faster speed on larger fibers and on all substrates after VE-cadherin blocking, consistent with a loss of contact inhibition by VE-cadherin. c) Correlation distance (mean radial distance at which mean cell-cell correlation equals 0; see Figure S9) decreased with increasing fiber width and after VE-cadherin blocking, indicating a loss of contact guidance by VE-cadherin on topographically varied substrates. d) Confocal images of ECs cultured on varied width ELP fibers with and without VE-cadherin blocking antibody, and stained for Ki67 (red; positive cell indicated by white arrow) and nuclei (blue). Fibers shown in violet. e) Quantification of Ki67 growth fraction per culture condition showed a VE-cadherin dependent increase in proliferation on larger width ELP fibers. (* p < 0.05, **p< 0.01,*** p< 0.001)