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@ARTICLE{DiMarco:164063,
author = {B. Di Marco$^*$ and E. E. Crouch and B. Shah and C.
Duman$^*$ and M. F. Paredes and C. Ruiz de Almodovar and E.
J. Huang and J. Alfonso$^*$},
title = {{R}eciprocal {I}nteraction between {V}ascular {F}ilopodia
and {N}eural {S}tem {C}ells {S}hapes {N}eurogenesis in the
{V}entral {T}elencephalon.},
journal = {Cell reports},
volume = {33},
number = {2},
issn = {2211-1247},
address = {[New York, NY]},
publisher = {Elsevier},
reportid = {DKFZ-2020-02231},
pages = {108256},
year = {2020},
note = {#EA:A231#LA:A231#},
abstract = {Angiogenesis and neurogenesis are tightly coupled during
embryonic brain development. However, little is known about
how these two processes interact. We show that nascent blood
vessels actively contact dividing neural stem cells by
endothelial filopodia in the ventricular zone (VZ) of the
murine ventral telencephalon; this association is conserved
in the human ventral VZ. Using mouse mutants with altered
vascular filopodia density, we show that this interaction
leads to prolonged cell cycle of apical neural progenitors
(ANPs) and favors early neuronal differentiation.
Interestingly, pharmacological experiments reveal that ANPs
induce vascular filopodia formation by upregulating vascular
endothelial growth factor (VEGF)-A in a cell-cycle-dependent
manner. This mutual relationship between vascular filopodia
and ANPs works as a self-regulatory system that senses ANP
proliferation rates and rapidly adjusts neuronal production
levels. Our findings indicate a function of vascular
filopodia in fine-tuning neural stem cell behavior, which is
the basis for proper brain development.},
cin = {A231},
ddc = {610},
cid = {I:(DE-He78)A231-20160331},
pnm = {311 - Signalling pathways, cell and tumor biology
(POF3-311)},
pid = {G:(DE-HGF)POF3-311},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:33053356},
doi = {10.1016/j.celrep.2020.108256},
url = {https://inrepo02.dkfz.de/record/164063},
}