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For example, if a monolayer of endothelial cells begins sprouting to form capillaries, angiogenesis is occurring. Vasculogenesis, in contrast, is when endothelial precursor cells (angioblasts) migrate and differentiate in response to local cues (such as growth factors and extracellular matrices) to form new blood vessels. These vascular trees ...
The cells that are proliferating are located behind the tip cells and are known as stalk cells. [12] The proliferation of these cells allows the capillary sprout to grow in length simultaneously. As sprouts extend toward the source of the angiogenic stimulus, endothelial cells migrate in tandem , using adhesion molecules called integrins .
Endothelial activation is a proinflammatory and procoagulant state of the endothelial cells lining the lumen of blood vessels. [1] It is most characterized by an increase in interactions with white blood cells (leukocytes), and it is associated with the early states of atherosclerosis and sepsis, among others. [2]
The endothelium (pl.: endothelia) is a single layer of squamous endothelial cells that line the interior surface of blood vessels and lymphatic vessels. [1] The endothelium forms an interface between circulating blood or lymph in the lumen and the rest of the vessel wall.
Neuroangiogenesis is finely regulated and sequential, involving proliferation and migration of endothelial cells to restore blood–brain barrier function, recruitment of pericytes, and stabilization new blood vessels, a process dependent on upregulation of proangiogenic factors, such as VEGF and angiopoietin-1.
Neovascularization is the natural formation of new blood vessels (neo-+ vascular + -ization), usually in the form of functional microvascular networks, capable of perfusion by red blood cells, that form to serve as collateral circulation in response to local poor perfusion or ischemia.
The blood–brain barrier (BBB) is a highly selective semipermeable border of endothelial cells that regulates the transfer of solutes and chemicals between the circulatory system and the central nervous system, thus protecting the brain from harmful or unwanted substances in the blood. [1]
When a cell is deficient in oxygen, it produces HIF, hypoxia-inducible factor, a transcription factor. HIF stimulates the release of VEGF-A, among other functions (including modulation of erythropoiesis). Circulating VEGF-A then binds to VEGF receptors on endothelial cells, triggering a tyrosine kinase pathway leading to angiogenesis.