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Low magnesium promotes endothelial cell dysfunction: implications for atherosclerosis, inflammation and thrombosis
Jeanette A M Maier1, Corinne Malpuech-Brugère, Wioletta Zimowska
1Department of Preclinical Sciences LITA Vialba, University of Milan, Via GB Grassi 74, 20157, Milan, Italy. jeanette.maier@unimi.it
Biochimica Et Biophysica Acta
|May 26, 2004
Summary
Low magnesium (Mg) impairs endothelial cell function, inhibiting proliferation and migration. This magnesium deficiency promotes inflammation and thrombosis, contributing to cardiovascular disease development.
Area of Science:
- Cardiovascular Biology
- Cellular Physiology
- Molecular Medicine
Background:
- Endothelial cells are critical in cardiovascular health.
- Magnesium (Mg) deficiency is linked to atherosclerosis, thrombosis, and hypertension.
Purpose of the Study:
- To investigate the direct impact of low magnesium concentrations on endothelial cell behavior.
- To elucidate the molecular mechanisms underlying magnesium deficiency-induced endothelial dysfunction.
Main Methods:
- Cultured endothelial cells were exposed to low magnesium concentrations.
- Cell proliferation, interleukin-1 (IL-1) levels, Vascular Cell Adhesion Molecule-1 (VCAM), Plasminogen Activator Inhibitor (PAI)-1, and gene expression were analyzed.
- Antisense oligonucleotide against IL-1 was used to block growth inhibition.
Main Results:
- Low Mg reversibly inhibited endothelial proliferation, correlating with decreased CDC25B levels.
- Interleukin-1 (IL-1) up-regulation mediated the growth inhibition.
- Magnesium deficiency increased VCAM and PAI-1 expression, enhancing monocytoid cell adhesion.
- Endothelial cell migration was impaired, with modulation of transcripts involved in adhesion and migration.
Conclusions:
- Low magnesium directly induces endothelial dysfunction.
- This dysfunction creates a pro-inflammatory, pro-thrombotic, and pro-atherogenic environment.
- Magnesium deficiency plays a role in the pathogenesis of cardiovascular diseases.