We need this to support any neurogenesis or stem cell treatment. But will not occur because we have NO stroke leadership or strategy.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=162678&CultureCode=en
How vascular tubes build, maintain and adapt continuously
perfused lumens to meet local metabolic needs remains poorly understood.
Recent studies showed that blood flow itself plays a critical role in
the remodelling of vascular networks and suggested it is also required
for the lumenization of new vascular connections. However, it is still
unknown how haemodynamic forces contribute to the formation of new
vascular lumens during blood vessel morphogenesis. An international team
of researchers under the direction of Holger Gerhardt (VIB/KU
Leuven/Cancer Research UK/MDC/BIH Berlin) found that blood flow drives
lumen expansion during sprouting angiogenesis in vivo by inducing
spherical deformations of the apical membrane of endothelial cells, in a
process that they have termed inverse blebbing.
Holger Gerhardt (VIB/KU Leuven/Cancer Research UK/ MDC/BIH Berlin):
“This work combined with previous studies highlights the importance of
balanced endothelial cell contractility in allowing the expansion and
maintenance of endothelial lumens during blood vessel development.”
These results challenge the previous idea that sprouting cells expand
lumens independently of blood flow during angiogenesis in vivo through
the generation and fusion of intracellular vacuoles. The researchers
showed that haemodynamic forces dynamically shape the apical membrane of
single or groups of endothelial cells during angiogenesis in vivo to
form and expand new lumenized vascular tubes. “We find that this
process relies on a tight balance between the forces applied on the
membrane and the local contractile responses from the endothelial cells,
as impairing this balance either way leads to lumen defects”, Holger
Gerhardt says.
This finding of inverse blebbing suggests that the process of
blebbing, best studied in cell migration and cytokinesis, does not
require a specific polarity, but is likely to be generally applicable to
situations in which external versus internal pressure differences
challenge the stability and elasticity of the actin cortex. It more
generally raises the question of the role of apical membrane
contractility in the adaptation to varying haemodynamic environments,
both during blood vessel morphogenesis, as connections form or remodel,
and in pathological settings.
Holger Gerhardt: “Understanding whether and how this plasticity of
the apical membrane and its underlying cortex is challenged in
pathological conditions, where vessels exhibit altered perfusion and
lack organized structure, has the potential to provide deeper insight
into mechanisms of vascular adaptation and maladaptation. We will
definitely further investigate this.”
Alongside the publication
of the Holger Gerhardt lab a highlight article from Erez Raz
(University of Münster, Institute of Cell Biology) was published. In
this article he concludes: ‘Overall, this work underscores the
significance of dynamic in vivo analysis for the understanding of
fundamental processes in cell and developmental biology. Employing
improved imaging techniques and the newly-developed powerful genetic
tools in the zebrafish model are likely to provide an even deeper
understanding of the mechanisms controlling vascular system development,
as well as those important for the formation and shaping of other
organs, tissues and structures.’
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