Gene Regulation in Endothelial Cells

Author(s):  
Scott L. Diamond ◽  
Larry V. Mcintire
Biomaterials ◽  
2004 ◽  
Vol 25 (21) ◽  
pp. 5137-5146 ◽  
Author(s):  
R.E. Unger ◽  
K. Peters ◽  
M. Wolf ◽  
A. Motta ◽  
C. Migliaresi ◽  
...  

2005 ◽  
Vol 21 (1) ◽  
pp. 124-130 ◽  
Author(s):  
Stacie R. Frye ◽  
Andrew Yee ◽  
Suzanne G. Eskin ◽  
Rudy Guerra ◽  
Xiuyu Cong ◽  
...  

Microarrays were utilized to determine gene expression of vascular endothelial cells (ECs) subjected to mechanical stretch for insight into the role of strain in vascular pathophysiology. Over 4,000 genes were screened for expression changes resulting from cyclic strain (10%, 1 Hz) of human umbilical vein ECs for 6 and 24 h. 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 h of cyclic stretch upregulated two genes and downregulated two genes, whereas 24 h of cyclic stretch upregulated eight genes but downregulated 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 threefold 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 at 24 h and plasminogen activator inhibitor 1 at 6 h. 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 ECs. However, many of the differentially expressed genes possess antioxidant properties, suggesting that oxidative mechanisms direct EC adaptation to cyclic stretch.


2005 ◽  
Vol 327 (3) ◽  
pp. 700-706 ◽  
Author(s):  
Kazue Shimizu ◽  
Kazuhide Watanabe ◽  
Hiroshi Yamashita ◽  
Mayumi Abe ◽  
Hironobu Yoshimatsu ◽  
...  

2005 ◽  
Vol 21 (3) ◽  
pp. 308-313 ◽  
Author(s):  
J. Gregory Maresh ◽  
Huaxia Xu ◽  
Nan Jiang ◽  
C. Gary Gairola ◽  
Ralph V. Shohet

We hypothesized that human smoking and its deleterious effects on endothelial function can be modeled by exposure of mice to tobacco smoke, and further that these changes would be reflected in gene regulation in vascular endothelium. We used for these studies a mouse strain that expresses green fluorescent protein under the control of an endothelial-specific promoter, Tie-2. Mice were exposed to sidestream smoke from reference cigarettes at 34 mg total suspended particulates/m3. After exposure for 5 days/wk for 1 and 6 wk, aortas were pooled from treatment and control groups. Endothelial cells were rapidly isolated by collagenase treatment followed by fluorescent activated cell sorting to yield populations of >95% purity. RNA isolated from >500 endothelial cells was amplified and analyzed on deeply representative long oligo microarrays. Transcripts dysregulated by >2.5-fold were confirmed by real-time PCR and selected proteins by immunofluorescent localization. In the endothelial cells, the observed more than threefold upregulation of complement factor H (Cfh), calcitonin receptor-like (Calcr1), and soluble epoxide hydrolase (Epxh2) may play a role in hypertensive responses of the vasculature to smoking. We have identified gene regulation in vivo in vascular endothelium that potentially underlies hypertensive responses to tobacco smoke.


2007 ◽  
Vol 77 (Suppl_1) ◽  
pp. 138-138
Author(s):  
Daniel Herr ◽  
Miriam Rodewald ◽  
Gerda Hack ◽  
Rolf Kreienberg ◽  
Christine Wulff

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