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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},
}