We need angiogenesis to supply blood to any migrating stem cells or migratory neurogenesis. Ask your doctor to translate and put into a useful stroke protocol. Unless you ask, nothing is going to get done.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0067029
Abstract
Aim
Accumulating
evidence suggests that extracellular galectin-1 and galectin-3 promote
angiogenesis. Increased expression of galectin-1 and/or galectin-3 has
been reported to be associated with tumour progression. Thus, it is
critical to identify their influence on angiogenesis.
Methods
We
examined the individual and combined effects of galectin-1 and
galectin-3 on endothelial cell (EC) growth and tube formation using two
EC lines, EA.hy926 and HUVEC. The activation of vascular endothelial
growth factor receptors (VEGFR1 and VEGFR2) was determined by ELISA and
Western blots. We evaluated the VEGFR1 and VEGFR2 levels in endosomes by
proximity ligation assay.
Results
We
observed different responses to exogenous galectins depending on the EC
line. An enhanced effect on EA.hy926 cell growth and tube formation was
observed when both galectins were added together. Focusing on this
enhanced effect, we observed that together galectins induced the
phosphorylation of both VEGFR1 and VEGFR2, whereas galectin-1 and −3
alone induced VEGFR2 phosphorylation only. In the same way, the addition
of a blocking VEGFR1 antibody completely abolished the increase in tube
formation induced by the combined addition of both galectins. In
contrast, the addition of a blocking VEGFR2 antibody only partially
inhibited this effect. Finally, the addition of both galectins induced a
decrease in the VEGFR1 and VEGFR2 endocytic pools, with a significantly
enhanced effect on the VEGFR1 endocytic pool. These results suggest
that the combined action of galectin-1 and galectin-3 has an enhanced
effect on angiogenesis via VEGFR1 activation, which could be related to a
decrease in receptor endocytosis.
No comments:
Post a Comment