Regeneration of blood vessels

A new study led by researchers identifies a signaling pathway that is essential for angiogenesis, the growth of new blood vessels from pre-existing vessels. The finding may improve current strategies to improve blood flow in ischemic tissue, such as that found in atherosclerosis and peripheral vascular disease associated with diabetes.

The research shows that the formation of fully functional blood vessels requires activation of protein kinase Akt by a protein called R-Ras, and this mechanism is necessary for the formation of the hallow structure, or lumen, of a blood vessel.This showed the biological process needed to increase blood flow in ischemic tissues.

Research team used a combination of 3D cell culture and living tissue to show that vascular endothelial growth factor VEGF promotes vascularization, but the vessel structures formed are chaotic, unstable and non-functional. Functional vessels need to have a lumen; a pipe-like opening that allows oxygenated blood and nutrients to travel through the body and VEGF alone cannot fully support the formation of such a vessel structure.

 VEGF activates Akt to induce endothelial cells to sprout. Then, R-Ras activates Akt to induce lumen formation. The second step involving Akt activation by R-Ras stabilizes the microtubule cytoskeleton in endothelial cells, creating a steady architecture that promotes lumen formation. VEGF and R-Ras activation of Akt signaling are complementary to each other, both are necessary to generate fully functional blood vessels to repair ischemic tissue.  
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Potassium regulates calcification of arteries

Foods rich in potassium like banana and avocado may protect against pathogenic vascular calcification.
Reduced dietary potassium promotes elevated aortic stiffness in a mouse model, as compared with normal-potassium-fed mice.

Arterial stiffness in humans is predictive of heart disease and death from heart disease, increased dietary potassium levels lessened vascular calcification and aortic stiffness. The different levels of dietary potassium were monitored by different blood levels of potassium in the three groups of mice.

When researchers looked at arterial cross-sections in cultures that were exposed to three different concentrations of potassium, based on normal physiological levels of potassium in the blood, they found a direct effect for the potassium on arterial calcification within arterial rings.

Arterial rings in low-potassium had markedly enhanced calcification, while high-potassium inhibited aortic calcification. In cell culture, low potassium levels in the culture media markedly enhanced calcification of vascular smooth muscle cells.

They discovered that the low-potassium conditions promoted the expression of several gene markers that are hallmarks of bone cells, but decreased the expression of vascular smooth muscle cell markers, suggesting the transformation of the vascular smooth muscle cells into bone-like cells under low-potassium conditions. They found that low-potassium increased intracellular calcium in the vascular smooth muscle cells, through a potassium transport channel called the inward rectifier potassium channel.
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