gms | German Medical Science

Joint-Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN) and the Scandinavian Neuropathological Society (SNS)

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie

22.09.-24.09.2016, Hamburg

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The role of EMT proteins in human brain vascular pericytes

Meeting Abstract

Suche in Medline nach

  • Jakob Ehlers - University of Tübingen, Hertie Institute for Clinical Brain Research, Vascular Neurology, Tübingen, Germany
  • Naita M. Wirsik - Edinger Institute, University of Frankfurt/Main, Neuropathology, Frankfurt/Main, Germany
  • Eva Blank - Edinger Institute, University of Frankfurt/Main, Neuropathology, Frankfurt/Main, Germany
  • Patrick N. Harter - Edinger Institute, University of Frankfurt/Main, Neuropathology, Frankfurt/Main, Germany
  • Michel Mittelbronn - Edinger Institute, University of Frankfurt/Main, Neuropathology, Frankfurt/Main, Germany
  • presenting/speaker Ulrike Naumann - University of Tübingen, Hertie Institute for Clinical Brain Research, Vascular Neurology, Tübingen, Germany

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie. Scandinavian Neuropathological Society. Joint-Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN) and the Scandinavian Neuropathological Society (SNS). Hamburg, 22.-24.09.2016. Düsseldorf: German Medical Science GMS Publishing House; 2016. Doc16dgnnP33

doi: 10.3205/16dgnn37, urn:nbn:de:0183-16dgnn372

Veröffentlicht: 14. September 2016

© 2016 Ehlers et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.

Gliederung

Text

Epithelial-to-mesenchymal transition (EMT) is accused to be responsible for increased invasion and metastases in epithelial cancer cells. Similar mechanisms have been proposed for primary CNS neoplasms, however there are only limited data for human brain tumors. Therefore, we are interested to decipher the cellular source of EMT factors and its clinico-pathological relevance in human gliomas. Using immunohistochemistry we identified SLUG and TWIST to be overexpressed in gliomas, however strongly related to tumors showing vascular proliferation such as pilocytic astrocytomas and glioblastomas. SLUG and TWIST are exclusively expressed in non-neoplastic pericytes covering glioma-associated blood vessels, but not in pericytes covering non-tumor associated vessels or in the tumor cells themselves. Treatment of primary human brain vascular pericytes (HBVP) with TGF-β or with TGFβ-containing supernatants from glioma cells leads to the upregulation of SNAIL and SLUG, paralleled by the induction of a star-like cellular network and the promotion of cell motility. In addition, these phenomena are also seen if HBPVS grow under hypoxic conditions. Consistent with these data, adenovirus-based overexpression of SLUG or SNAIL in HBVPs also transfers into morphological changes. The morphological changes in HBVPs coincide with the induction of alpha smooth muscle actin (α-SMA), a protein known to be upregulated in brain pericyteslocated in proximity to glioma tissue. We believe that identifying the role of pericytes in the microenvironment of GBM will provide promising new aspects for the treatment of GBM.