% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Schneller:142851,
author = {D. Schneller$^*$ and R. Hofer-Warbinek and C. Sturtzel and
K. Lipnik and B. Gencelli and M. Seltenhammer and M. Wen and
J. Testori and M. Bilban and A. Borowski and M. Windwarder
and S. Kapel$^*$ and E. Besemfelder$^*$ and P. Cejka and A.
Habertheuer and B. Schlechta and O. Majdic and F. Altmann
and A. Kocher and H. Augustin$^*$ and W. Luttmann and E.
Hofer},
title = {{C}ytokine-{L}ike 1 {I}s a {N}ovel {P}roangiogenic {F}actor
{S}ecreted by and {M}ediating {F}unctions of {E}ndothelial
{P}rogenitor {C}ells.},
journal = {Circulation research},
volume = {124},
number = {2},
issn = {1524-4571},
address = {New York, NY},
publisher = {Assoc.},
reportid = {DKFZ-2019-00481},
pages = {243 - 255},
year = {2019},
note = {DKFZ-ZMBH Alliance},
abstract = {Endothelial colony forming cells (ECFCs) or late blood
outgrowth endothelial cells can be isolated from human cord
or peripheral blood, display properties of endothelial
progenitors, home into ischemic tissues and support
neovascularization in ischemic disease models.To assess the
functions of CYTL1 (cytokine-like 1), a factor we found
preferentially produced by ECFCs, in regard of vessel
formation.We show by transcriptomic analysis that ECFCs are
distinguished from endothelial cells of the vessel wall by
production of high amounts of CYTL1. Modulation of
expression demonstrates that the factor confers increased
angiogenic sprouting capabilities to ECFCs and can also
trigger sprouting of mature endothelial cells. The data
further display that CYTL1 can be induced by hypoxia and
that it functions largely independent of VEGF-A (vascular
endothelial growth factor-A). By recombinant production of
CYTL1 we confirm that the peptide is indeed a strong
proangiogenic factor and induces sprouting in cellular
assays and functional vessel formation in animal models
comparable to VEGF-A. Mass spectroscopy corroborates that
CYTL1 is specifically O-glycosylated on 2 neighboring
threonines in the C-terminal part and this modification is
important for its proangiogenic bioactivity. Further
analyses show that the factor does not upregulate
proinflammatory genes and strongly induces several
metallothionein genes encoding anti-inflammatory and
antiapoptotic proteins.We conclude that CYTL1 can mediate
proangiogenic functions ascribed to endothelial progenitors
such as ECFCs in vivo and may be a candidate to support
vessel formation and tissue regeneration in ischemic
pathologies.},
cin = {A100 / A190},
ddc = {610},
cid = {I:(DE-He78)A100-20160331 / I:(DE-He78)A190-20160331},
pnm = {321 - Basic Concepts (POF3-321)},
pid = {G:(DE-HGF)POF3-321},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:30582450},
doi = {10.1161/CIRCRESAHA.118.313645},
url = {https://inrepo02.dkfz.de/record/142851},
}