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J Cell Sci. 2006 Oct 1;119(Pt 19):4127-37. Epub 2006 Sep 12.

Silencing profilin-1 inhibits endothelial cell proliferation, migration and cord morphogenesis.

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  • 1Department of Bioengineering, University of Pittsburgh, 749 Benedum Hall, 3700 O'Hara Street, Pittsburgh, PA 15261, USA.

Erratum in

  • J Cell Sci. 2006 Oct 15;119(Pt 20):4366.


Expression of several actin-binding proteins including profilin-1 is up-regulated during capillary morphogenesis of endothelial cells, the biological significance of which remains unknown. Specifically, we hypothesized that profilin-1 is important for endothelial migration and proliferation. In this study, we suppressed profilin-1 expression in human umbilical vein endothelial cells by RNA-interference. Gene silencing of profilin-1 led to significant reduction in the formation of actin filaments and focal adhesions. Loss of profilin-1 expression was also associated with reduced dynamics of cell-cell adhesion. Data from both wound-healing experiments and time-lapse imaging of individual cells showed inhibition of cell migration when profilin-1 expression was suppressed. Cells lacking profilin-1 exhibited defects in membrane protrusion, both in terms of its magnitude and directional persistence. Furthermore, loss of profilin-1 expression inhibited cell growth without compromising cell survival, at least in the short-term, thus suggesting that profilin-1 also plays an important role in endothelial proliferation as hypothesized. Finally, silencing profilin-1 expression suppressed matrigel-induced early cord morphogenesis of endothelial cells. Taken together, our data suggest that profilin-1 may play important role in biological events that involve endothelial proliferation, migration and morphogenesis.

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