scholarly journals Cyclooxygenase-2 Induction and Prostacyclin Release by Protease-activated Receptors in Endothelial Cells Require Cooperation between Mitogen-activated Protein Kinase and NF-κB Pathways

2006 ◽  
Vol 281 (17) ◽  
pp. 11792-11804 ◽  
Author(s):  
Farisa Syeda ◽  
Jennifer Grosjean ◽  
Rebecca A. Houliston ◽  
Rosemary J. Keogh ◽  
Tom D. Carter ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase ◽  
Cyclooxygenase 2 ◽  
Mitogen Activated Protein Kinase ◽  
Protease Activated Receptors ◽  
Mitogen Activated Protein

scholarly journals Glyoxal Damages Human Aortic Endothelial Cells by Perturbing the Glutathione, Mitochondrial Membrane Potential, and Mitogen-Activated Protein Kinase Pathways

2021 ◽  
Author(s):  
Ming-Zhang Xie ◽  
Chun Guo ◽  
Jia-Qi Dong. BA ◽  
Jie Zhang ◽  
Ke-Tao Sun ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Membrane Potential ◽  
Protein Kinase ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Mitogen Activated Protein Kinase ◽  
Aortic Endothelial Cells ◽  
Mitogen Activated Protein ◽  
Human Aortic Endothelial Cells ◽  
Quantitative Fluorescence

Abstract Background: Exposure to glyoxal, the smallest dialdehyde, is associated with several diseases; humans are routinely exposed to glyoxal because of its ubiquitous presence in foods and the environment. The aim of this study was to examine the damage caused by glyoxal in human aortic endothelial cells. Methods: Cell survival assays and quantitative fluorescence assays were performed to measure DNA damage; oxidative stress was detected by colorimetric assays and quantitative fluorescence, and the mitogen-activated protein kinase pathways were assessed using western blotting. Results: Exposure to glyoxal was found to be linked to abnormal glutathione activity, the collapse of mitochondrial membrane potential, and the activation of mitogen-activated protein kinase pathways. However, DNA damage and thioredoxin oxidation were not induced by dialdehydes. Conclusions: Intracellular glutathione, members of the mitogen-activated protein kinase pathways, and the mitochondrial membrane potential are all critical targets of glyoxal. These findings provide novel insights into the molecular mechanisms perturbed by glyoxal and may facilitate the development of new therapeutics and diagnostic markers for cardiovascular diseases.

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