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@MISC{Mller:282928,
author = {Müller, Stephan A and Lichtenthaler, Stefan},
title = {{D}ataset: {M}ass-spectrometry analysis of brain
endothelial cells ({BEC}s) from {F}oxf2i{ECKO} and {C}trl
mice ({P}roject {PXD}051839)},
publisher = {PRoteomics IDEntifications Database},
reportid = {DZNE-2025-01389},
year = {2025},
abstract = {To identify the molecular and cellular pathways mediating
the effects of Foxf2 in brain endothelial cells (BECs), we
performed proteomic analysis of mouse BECs. For this, we
applied our previously published BEC enrichment protocol
using magnetic-activated cell sorting (MACS) combined with
liquid chromatography-mass spectrometry (LC-MS/MS) based
proteomics (Todorov-Völgyi et al., 2024) to 6 months old
animals. Proteomic analysis of isolated BECs captured a
total of 4750 proteins. Out of these, 320 and 434 proteins
were significantly up-, and downregulated, respectively in
Cdh5-CreERT2;Foxf2fl/fl (Foxf2iECKO) vs Foxf2fl/fl (Ctrl)
mice. In GO enrichment analyses of significantly
downregulated proteins we found ‘establishment of
endothelial barrier’, ‘nitric oxide metabolic process’
and ‘positive regulation of angiogenesis’ to be among
the most affected categories. Fold-change ranking of
significantly altered proteins marked Tie2 as one of the
most strongly downregulated proteins. Notably, several
proteins involved in Tie2-regulated processes, including
Nos3 and Ptgis (implicated in nitric oxide metabolic
process), Rap1b, Tjp1, Cldn5, and Cdh5 (implicated in
establishment of endothelial barrier), and Tie2, Eng, and
Itgb1 (implicated in angiogenesis) were downregulated in
BECs from Foxf2iECKO mice. Collectively, these findings
demonstrate a critical role of endothelial Foxf2 in
maintaining BBB integrity and Tie2 signaling.},
cin = {AG Lichtenthaler},
cid = {I:(DE-2719)1110006},
pnm = {352 - Disease Mechanisms (POF4-352)},
pid = {G:(DE-HGF)POF4-352},
typ = {PUB:(DE-HGF)32},
url = {https://pub.dzne.de/record/282928},
}