| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Bioengineering, Rice University, Houston, TX, USA
2 Department of Bioengineering, Rice University, Houston, TX, USA; Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology/Emory University, Atlanta, GA, USA
3 Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology/Emory University, Atlanta, GA, USA
4 Department of Statistics, Rice University, Houston, TX, USA
* To whom correspondence should be addressed. E-mail: larry.mcintire{at}bme.gatech.edu.
Microarrays were utilized to determine gene expression of vascular endothelial cells subjected to mechanical stretch for insight into the role of strain in vascular pathophysiology. Over 4000 genes were screened for expression changes resulting from cyclic strain (10%, 1 Hertz) of human umbilical vein endothelial cells for 6 and 24 hours. Comparison of t-statistics and adjusted p-values identified genes having significantly different expression between strained and static cells, but not between strained and motion control. Relative to static, 6 hours of cyclic stretch up-regulated 2 genes and down-regulated 2 genes, whereas 24 hours of cyclic stretch up-regulated 8 genes but down-regulated no genes. However, incorporating the motion control revealed that fluid agitation over the cells, rather than strain, is the primary regulator of differential expression. Furthermore, no gene exceeded a 3-fold change when comparing cyclic strain to either static or motion control. Quantitative real-time polymerase chain reaction confirmed the dominance of fluid agitation in gene regulation with the exception of heat shock protein 10 (HSP10) at 24 hours and plasminogen activator inhibitor 1 (PAI-1) at 6 hours. Taken together, the small number of differentially expressed genes and their low fold-expression levels indicate that cyclic strain is a weak inducer of gene regulation in endothelial cells. However, many of the differentially expressed genes possess antioxidant properties, suggesting that oxidative mechanisms direct endothelial cell adaptation to cyclic stretch.
This article has been cited by other articles:
|
|
 |
|
  H.-J. Sung, A. Yee, S. G. Eskin, and L. V. McIntire Cyclic strain and motion control produce opposite oxidative responses in two human endothelial cell types Am J Physiol Cell Physiol, July 1, 2007; 293(1): C87 - C94. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. A. Bundey Endothelial cell mechanosensitivity. Focus on "Cyclic strain and motion control produce opposite oxidative responses in two human endothelial cell types" Am J Physiol Cell Physiol, July 1, 2007; 293(1): C33 - C34. [Full Text] [PDF]
|
|
|
|
 |
|
 P. M. Cummins, N. von Offenberg Sweeney, M. T. Killeen, Y. A. Birney, E. M. Redmond, and P. A. Cahill Cyclic strain-mediated matrix metalloproteinase regulation within the vascular endothelium: a force to be reckoned with Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H28 - H42. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
