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Journal of Nanomaterials
Volume 2013, Article ID 251063, 10 pages
http://dx.doi.org/10.1155/2013/251063
Research Article

Enhanced Ca2+ Entry and Tyrosine Phosphorylation Mediate Nanostructure-Induced Endothelial Proliferation

1Institute of Biophysics, Medical University Graz, 8010 Graz, Austria
2Department of Cell Biology, Histology and Embryology, Core Facility Ultrastructure Analysis, Center for Medical Research, Medical University Graz, 8010 Graz, Austria
3Institute of Molecular Biosciences, University of Graz, 8010 Graz, Austria
4Institute of Applied Physics, Johannes Kepler University Linz, 4040 Linz, Austria
5Institute of Molecular Biology and Biochemistry, Medical University Graz, 8010 Graz, Austria

Received 23 August 2013; Accepted 6 October 2013

Academic Editor: Krasimir Vasilev

Copyright © 2013 Michaela Schernthaner et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Supplementary Material

Supplement Figure 1: According to the findings that β-catenin translocates to the nucleus in HMEC grown on nanostructured substrates, the stability of endothelial cell-cell contacts build up by adherens junctions was questionable. β-catenin is usually bound intracellularly to VE-cadherin, the main protein forming adherens junctions, linking the cells to each other via its extracellular domain. To test for intactness of adherens junctions, HMEC were fixed and immunostained with an antibody against VE-cadherin. The protein is located in contact sites of the plasma membrane of neighboring cells, confirming the presence of junctional contacts.

Supplement Figure 2: Due to the lack of signal intensity for HMEC grown wall structures with the cells stained against FAK phosphorylated on site 397, the images of Figure 3 are shown here with excessively enhanced brightness. It is evident from the bright images that the substrates were covered with cells and the low signal intensity is resulting probably from the lack of focal adhesions formed on wall structured substrates.

Supplement Figure 3: The proliferation levels of HMEC grown on the nanostructured substrates incubated with different inhibitors were determined via immunofluorescence levels of the proliferation marker Ki 67. Representative images used for the quantitative analysis of the mean nuclear fluorescence in Figure 6 are shown.

  1. Supplementary Figures