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Copper-homocysteine complexes and potential physiological actions.
Margarita D Apostolova1, Panayot R Bontchev, Bojidarka B Ivanova
1Department of Cellular Integrity, Rowett Research Institute, Aberdeen AB219SB, UK. m.apostolova@utoronto.ca
Journal of Inorganic Biochemistry
|June 24, 2003
Summary
Copper-homocysteine complexes influence extracellular thiol metabolism and endothelial cell interactions, potentially contributing to atherosclerosis development. These complexes impact monocyte adhesion and diapedesis, suggesting a role in atherogenesis.
Area of Science:
- Biochemistry
- Cell Biology
- Cardiovascular Research
Background:
- Atherogenesis is linked to homocysteine (hCys) and copper (Cu) homeostasis.
- The physiological role of hCys may involve complex formation with Cu.
Purpose of the Study:
- To investigate the formation and biological effects of copper-homocysteine (Cu-hCys) complexes.
- To determine the impact of Cu-hCys complexes on endothelial cell function and atherogenesis.
Main Methods:
- Characterization of Cu-hCys complexes using spectroscopy and coordination chemistry.
- Assay of extracellular thiol metabolism and glutathione peroxidase-1 activity.
- Analysis of focal adhesion complex remodeling, paxillin phosphorylation, and monocyte-endothelial cell interactions.
Main Results:
- Two distinct Cu-hCys complexes were identified: a blue Cu(II)-hCys complex and a yellow Cu(I)-hCys complex.
- Both complexes altered extracellular thiol metabolism and inhibited glutathione peroxidase-1.
- Cu-hCys complexes induced paxillin redistribution and enhanced monocyte diapedesis through endothelial cells.
Conclusions:
- Cu-hCys complexes actively modulate endothelial cell responses relevant to atherogenesis.
- These complexes influence monocyte adhesion and transmigration, key events in the development of atherosclerosis.
- Further research into Cu-hCys complexes may reveal novel therapeutic targets for cardiovascular disease.