Cyclic stretch-induced glutathione peroxidase-1 expression protects human endothelial cells against oxidative stress and pro-inflammatory gene expression

2006 ◽  
Vol 45 (3) ◽  
pp. e5-e6
Author(s):  
A.H. Wagner ◽  
O. Kautz ◽  
K. Fricke ◽  
F. Grimm ◽  
M. Hecker
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Endothelial Cells ◽  
Glutathione Peroxidase ◽  
Cyclic Stretch ◽  
Human Endothelial Cells ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Glutathione Peroxidase 1

scholarly journals TRAIL Induces Apoptosis and Inflammatory Gene Expression in Human Endothelial Cells

2003 ◽  
Vol 171 (3) ◽  
pp. 1526-1533 ◽  
Author(s):  
Jie Hui Li ◽  
Nancy C. Kirkiles-Smith ◽  
Jennifer M. McNiff ◽  
Jordan S. Pober
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Human Endothelial Cells ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene

scholarly journals Deciphering Regulatory Patterns of Inflammatory Gene Expression From Interleukin-1—Stimulated Human Endothelial Cells

2004 ◽  
Vol 24 (7) ◽  
pp. 1192-1198 ◽  
Author(s):  
Herbert Mayer ◽  
Martin Bilban ◽  
Vladislav Kurtev ◽  
Florian Gruber ◽  
Oswald Wagner ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Interleukin 1 ◽  
Human Endothelial Cells ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene

Changes in inflammatory gene expression induced by hyperbaric oxygen treatment in human endothelial cells under chronic wound conditions

2012 ◽  
Vol 318 (3) ◽  
pp. 207-216 ◽  
Author(s):  
Alexandra C. Kendall ◽  
Jacqueline L. Whatmore ◽  
Lorna.W. Harries ◽  
Paul G. Winyard ◽  
Gary R. Smerdon ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Hyperbaric Oxygen ◽  
Chronic Wound ◽  
Human Endothelial Cells ◽  
Hyperbaric Oxygen Treatment ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Oxygen Treatment

scholarly journals Cytoprotection of human endothelial cells from oxidative stress by polyphenols: the role of gene expression versus direct antioxidant effect

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Xinyu Wang ◽  
James Bynum ◽  
Salomon Stavchansky ◽  
Michael Dubick ◽  
Robert Hackman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Endothelial Cells ◽  
Antioxidant Effect ◽  
Human Endothelial Cells

scholarly journals Enhanced vulnerability to oxidative stress and induction of inflammatory gene expression in 3‐phosphoglycerate dehydrogenase‐deficient fibroblasts

FEBS Open Bio ◽  
2018 ◽  
Vol 8 (6) ◽  
pp. 914-922 ◽  
Author(s):  
Momoko Hamano ◽  
Yurina Haraguchi ◽  
Tomoko Sayano ◽  
Chong Zyao ◽  
Yashiho Arimoto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Phosphoglycerate Dehydrogenase

Oxidative stress and macrophage function: a failure to resolve the inflammatory response

2007 ◽  
Vol 35 (2) ◽  
pp. 284-287 ◽  
Author(s):  
P. Kirkham
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Inflammatory Response ◽  
Carbonyl Stress ◽  
Apoptotic Cells ◽  
Inflammatory Gene Expression ◽  
Macrophage Function ◽  
Inflammatory Gene ◽  
Ecm Proteins ◽  
Inflammatory State

The suppression of pro-inflammatory gene expression along with the clearance of apoptotic cells by phagocytosis can play an important role in resolving the inflammatory response. Any impairment of these processes can therefore lead to a chronic inflammatory state. Oxidative stress can have both direct and indirect effects on macrophage function. This mini-review highlights a mechanism through which oxidative stress via the production of reactive carbonyls alters the ECM (extracellular matrix) environment of macrophages, thereby altering their behaviour. Carbonyl modification of ECM proteins causes increased macrophage adhesion and activation through receptors that are also involved in phagocytosis. Moreover, interaction of macrophages with these carbonyl-modified ECM proteins leads to decreased phagocytic activity towards apoptotic cells. At a more direct level, both oxidative and carbonyl stress inhibits activity of the transcriptional co-repressor HDAC-2 (histone deacetylase 2), which under normoxic conditions helps to suppress pro-inflammatory gene expression. Consequently, macrophages activated under conditions of oxidative or carbonyl stress can lead to a more enhanced inflammatory response. Coupled with an impairment of the phagocytic response, this can lead to ineffective clearance of apoptotic cells and secondary necrosis, with the result being failure to resolve the inflammatory response and the establishment of a chronic inflammatory state.

Shear stress and KLF2 suppress basal inflammatory gene expression in endothelial cells by inhibiting ATF-2

2006 ◽  
Vol 45 (3) ◽  
pp. 178-179
Author(s):  
J.O. Fledderus ◽  
J.V. van Thienen ◽  
R.A. Boon ◽  
R.J. Dekker ◽  
A.P.J.J. Bijnens ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene
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