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@ARTICLE{Hasanov:124357,
author = {Z. Hasanov$^*$ and T. Ruckdeschel$^*$ and C. König$^*$ and
C. Mogler$^*$ and S. Kapel$^*$ and C. Korn$^*$ and C.
Spegg$^*$ and V. Eichwald$^*$ and M. Wieland$^*$ and S.
Appak$^*$ and H. Augustin$^*$},
title = {{E}ndosialin {P}romotes {A}therosclerosis {T}hrough
{P}henotypic {R}emodeling of {V}ascular {S}mooth {M}uscle
{C}ells.},
journal = {Arteriosclerosis, thrombosis, and vascular biology},
volume = {37},
number = {3},
issn = {1524-4636},
address = {Philadelphia, Pa.},
publisher = {Lippincott, Williams $\&$ Wilkins},
reportid = {DKFZ-2017-01236},
pages = {495 - 505},
year = {2017},
abstract = {Vascular smooth muscle cells (VSMC) play a key role in the
pathogenesis of atherosclerosis, the globally leading cause
of death. The transmembrane orphan receptor endosialin
(CD248) has been characterized as an activation marker of
cells of the mesenchymal lineage including tumor-associated
pericytes, stromal myofibroblasts, and activated VSMC. We,
therefore, hypothesized that VSMC-expressed endosialin may
display functional involvement in the pathogenesis of
atherosclerosis.Expression of endosialin was upregulated
during atherosclerosis in apolipoprotein E (ApoE)-null mice
and human atherosclerotic samples analyzed by quantitative
real-time polymerase chain reaction and
immunohistochemistry. Atherosclerosis, assessed by Oil Red O
staining of the descending aorta, was significantly reduced
in ApoE/endosialin-deficient mice on Western-type diet.
Marker analysis of VSMC in lesions induced by shear
stress-modifying cast implantation around the right carotid
artery identified a more pronounced contractile VSMC
phenotype in the absence of endosialin. Moreover, in
addition to contributing to neointima formation, endosialin
also potentially regulated the proinflammatory phenotype of
VSMC as evidenced in surrogate cornea pocket assay
experiments in vivo and corresponding flow cytometry and
ELISA analyses in vitro.The experiments identify endosialin
as a potential regulator of phenotypic remodeling of VSMC
contributing to atherosclerosis. The association of
endosialin with atherosclerosis and its absent expression in
nonatherosclerotic samples warrant further consideration of
endosialin as a therapeutic target and biomarker.},
keywords = {Antigens, CD (NLM Chemicals) / Antigens, Neoplasm (NLM
Chemicals) / Apolipoproteins E (NLM Chemicals) / CD248
protein, human (NLM Chemicals) / Neoplasm Proteins (NLM
Chemicals) / tumor endothelial marker 1, mouse (NLM
Chemicals)},
cin = {A190 / L101},
ddc = {610},
cid = {I:(DE-He78)A190-20160331 / I:(DE-He78)L101-20160331},
pnm = {321 - Basic Concepts (POF3-321)},
pid = {G:(DE-HGF)POF3-321},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:28126825},
doi = {10.1161/ATVBAHA.116.308455},
url = {https://inrepo02.dkfz.de/record/124357},
}