Deans' stroke musings: Membrane Trafficking and Endothelial-Cell Dynamics During Angiogenesis

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, March 7, 2012

Membrane Trafficking and Endothelial-Cell Dynamics During Angiogenesis

Only 28 pages and I learned something new, vasculogenesis vs angiogenesis, I wonder which is more applicable for us survivors that have lots of dead area. Cool diagrams in the pdf, sections listed, details at the link.
http://cdn.intechweb.org/pdfs/31164.pdf
1. Introduction
The formation of new blood vessels, or neovascularization, involves multiple processes,
including cell proliferation and migration, cell-cell and cell-matrix adhesion, and tube
morphogenesis. Neovascularization can occur through one of two events: vasculogenesis,
the de novo formation of blood vessels from angioblasts; or angiogenesis, the extension of
new vessels from a pre-existing vasculature. Among these, angiogenesis in particular is
relevant throughout life; its dysregulation has been causally related to several disorders that
involve malignancy, inflammation, and ischemia. Angiogenesis is thought to depend on a
set of signaling proteins – including certain kinases, integrins and vascular endothelial
growth factor receptor-2 (VEGFR2) – that are enriched in specific plasma membrane
domains. Both physiological and pathological angiogenesis rely on intracellular trafficking,
a process that governs signaling by such proteins, as well as cell motility.
In this chapter, we discuss our current understanding of angiogenesis from the perspective
of trafficking of the membrane components that are responsible for endothelial-cell (EC) dynamics.
2. Angiogenesis: Mechanism and importance

Fig. 1. Schematic representation of a mature blood vessel. Endothelial cells at the luminal
side line tubular blood vessel. The smooth muscle cells and the pericytes that remain in
contact with the endothelial cell lining through the basement membrane strengthen this
tubular structure.
2.1 Vasculogenesis
2.2 Angiogenesis
2.3 Pathological angiogenesis
3. Ligands and receptors in angiogenesis
3.1 The VEGF-VEGFR system coordinates the process of angiogenesis
3.1.1 VEGF
3.2 VEGF receptors
3.2.1 VEGFR1
3.2.2 VEGFR2
3.2.3 VEGFR3
3.2.4 Neuropilins (NRP)
3.3 Role of the extracellular matrix (ECM) in endothelial-cell interactions during angiogenesis
3.4 Role of Integrin in endothelial-cell dynamics during angiogenesis
4. Membrane trafficking
4.1 Biosynthetic/secretory pathway
4.2 Endocytic and exocytic pathways
4.3 Endocytic trafficking of VEGFR2
4.4 Secretory transport of VEGFR2
4.5 VEGFR2 trafficking and angiogenesis