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Physiol. Genomics (October 8, 2002). doi:10.1152/physiolgenomics.00068.2002
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Articles in PresS, published online ahead of print October 8, 2002
Physiol Genomics, 10.1152/physiolgenomics.00068.2002
Submitted on June 3, 2002
Accepted on September 30, 2002

VEGF-C MEDIATES CYCLIC PRESSURE-INDUCED ENDOTHELIAL CELL PROLIFERATION

Hainsworth Y Shin1, Michael L Smith2, Karen J Toy3, P. Mickey Williams3, Rena Bizios4*, and Mary E Gerritsen5

1 Department of Biomedical Engineering, Rensselaer Polytechnic Institute, Troy, NY, USA; Department of Molecular Biology and Department of Cardiovascular Research, Genentech, Incorporated, South San Francisco, CA, USA
2 Department of Molecular Biology and Department of Cardiovascular Research, Genentech, Incorporated, South San Francisco, CA, USA; Department of Biomedical Engineering, University of Virginia, Charlottesvile, VA, USA
3 Department of Molecular Biology and Department of Cardiovascular Research, Genentech, Incorporated, South San Francisco, CA, USA
4 Department of Biomedical Engineering, Rensselaer Polytechnic Institute, Troy, NY, USA
5 Department of Molecular Biology and Department of Cardiovascular Research, Genentech, Incorporated, South San Francisco, CA, USA; Department of Vascular Biology, Millennium Pharmaceuticals Inc., South San Francisco, CA, USA

* To whom correspondence should be addressed. E-mail: bizios{at}rpi.edu.

Mechanical forces modulate endothelial cell functions through several mechanisms including regulation of gene transcription. In the present study, gene transcription by human umbilical vein endothelial cells (HUVEC) either maintained under control pressure (that is, standard cell culture conditions equivalent to 0.15 mm Hg sustained hydrostatic pressure) or exposed to 60/20 mm Hg sinusoidal pressures at 1 Hz were compared using Affymetrix Genechip® microarrays in order to identify cellular/molecular mechanisms associated with endothelial cell responses to cyclic pressure. Cyclic pressure selectively affected transcription of 14 genes that included a set of mechanosensitive proteins involved in haemostasis (tissue plasminogen activator), cell adhesion (integrin {alpha}2), and cell signaling (Rho B, cytosolic phospholipase A2) as well as a unique subset of cyclic pressure-sensitive genes such as vascular endothelial growth factor (VEGF)-C and transforming growth factor-B2. The present study also provided first evidence that VEGF-C, the most highly-induced gene under 60/20 mm Hg, mediated HUVEC proliferation in response to this pressure. Cyclic pressure is, therefore, a mechanical force that modulates endothelial cell functions (such as proliferation) by activating a specific transcriptional program.




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[Abstract] [PDF]


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