Biomedical Engineering Reference
In-Depth Information
called just VEGF. A number of VEGF-related proteins have also been dis-
covered encoded by viruses (VEGF-E) and in the venom of some snakes
(VEGF-F). It is the part of the system that restores the oxygen supply
to tissues when blood circulation is inadequate. Serum concentration of
VEGF is high in bronchial asthma and low in diabetes mellitus. VEGF's
normal function is to create new blood vessels during embryonic develop-
ment, new blood vessels after injury, muscle following exercise, and new
vessels (collateral circulation) to bypass blocked vessels. When VEGF is
overexpressed, it can contribute to disease. Solid cancers cannot grow
beyond a limited size without an adequate blood supply; cancers that
can express VEGF are able to grow and metastasize. Overexpression of
VEGF can cause vascular disease in the retina of the eye and other parts
of the body. Drugs such as bevacizumab can inhibit VEGF and control
or slow those diseases. VEGF is a subfamily of growth factors, to be
specific, the platelet-derived growth factor family of cystine-knot growth
factors. They are important signaling proteins involved in both vasculo-
genesis (the de novo formation of the embryonic circulatory system) and
angiogenesis (the growth of blood vessels from preexisting vasculature).
All members of the VEGF family stimulate cellular responses by binding
to tyrosine kinase receptors (the VEGFRs) on the cell surface, causing
them to dimerize and become activated through transphosphorylation, al-
though to different sites, times, and extents. The VEGF receptors have an
extracellular portion consisting of 7 immunoglobulin-like domains, a single
transmembrane spanning region, and an intracellular portion containing
a split tyrosine-kinase domain. VEGF-A binds to VEGFR-1 (Flt-1) and
VEGFR-2 (KDR/Flk-1). VEGFR-2 appears to mediate almost all of the
known cellular responses to VEGF. The function of VEGFR-1 is less well
defined, although it is thought to modulate VEGFR-2 signaling. Another
function of VEGFR-1 may be to act as a dummy/decoy receptor, seques-
tering VEGF from VEGFR-2 binding (this appears to be particularly
important during vasculogenesis in the embryo). VEGF-C and VEGF-
D, but not VEGF-A, are ligands for a third receptor (VEGFR-3), which
mediates lymphangiogenesis.
Wound healing assay: Experimental model able to evaluate the migratory
phenotype of a cell population. It consists in the incubation of the cell
culture of interest toward confluence, and in the subsequent creation of
an artificial scratch with a sharp object (for example, a pipette tip). The
removal of cells from the wounded area acts as a stimulus for the re-
maining mass to invade and fill the open space, with a characteristic
traveling-wave-like behavior. The rate of advance of the wound edge, i.e.,
the quantification of the area recolonized, gives a measure of the migratory
capacity of the overall population. In particular, this technique is widely
used to compare the motility properties of a cell line either in resting
conditions (i.e., in the absence of any external stimuli) and in response to
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