Low magnesium concentrations inhibited microvascular endothelial cell growth and migration while increasing the synthesis of inflammatory markers including IL-1α, IL-6, nitric oxide, and VCAM.
Does magnesium concentration modulate inflammation and angiogenesis in microvascular endothelial cells?
Magnesium directly modulates microvascular endothelial cell functions, with low levels promoting inflammation and high levels promoting angiogenesis.
p-value: p=<0.05
Microvascular endothelial cells are protagonists in inflammation and angiogenesis. Since magnesium (Mg) deficiency promotes inflammation and impairs angiogenesis in vivo, we evaluated the effect of different concentrations of the cation on microvascular 1G11 cells. We found that low Mg inhibits endothelial growth and migration, while it increases some inflammatory markers. In particular we show that low Mg stimulates the synthesis of interleukin 1a and 6, of nitric oxide, a mediator of inflammatory responses, and of VCAM, which mediates monocyte/endothelial interactions. On the contrary, high Mg stimulates proliferation and migration and sensitizes microvascular cells to migratory signals, thus inducing crucial events in angiogenesis. Our results demonstrate a direct role of Mg in modulating microvascular functions and provide a molecular explanation to the link among Mg, angiogenesis and inflammation observed in in vivo models.
Daniela Bernardini (Sat,) conducted a other in Inflammation and angiogenesis. Magnesium vs. 1.0 mM Mg (physiological) was evaluated on Cell proliferation, migration, and inflammatory marker synthesis (p=<0.05). Low magnesium concentrations inhibited microvascular endothelial cell growth and migration while increasing the synthesis of inflammatory markers including IL-1α, IL-6, nitric oxide, and VCAM.