gms | German Medical Science

26. Jahrestagung der Deutschen Retinologischen Gesellschaft

Deutsche Gesellschaft für Retinologie

27.09.2013, Hamburg

Semaphorin 3F forms an anti-angiogenic barrier in the outer retina

Meeting Abstract

  • Andreas Stahl - Freiburg, Germany
  • A. Buehler - Freiburg, Germany
  • F. Bucher - Freiburg, Germany
  • S. Berger - Freiburg, Germany
  • A. Pielen - Freiburg, Germany
  • G. Martin - Freiburg, Germany
  • G. Schlunck - Freiburg, Germany
  • H.T. Agostini - Freiburg, Germany
  • P. Sapieha - Montreal, Canada
  • M. Klagsbrun - Vascular Biology Program, Harvard Medical School, Children's Hospital Boston, USA
  • L.E.H. Smith - Department of Ophthalmology, Harvard Medical School, Children's Hospital Boston, USA

Retinologische Gesellschaft. 26. Jahrestagung der Retinologischen Gesellschaft. Hamburg, 27.-27.09.2013. Düsseldorf: German Medical Science GMS Publishing House; 2013. Doc13rg06

doi: 10.3205/13rg06, urn:nbn:de:0183-13rg068

Veröffentlicht: 20. August 2013

© 2013 Stahl et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Background: Semaphorins are known modulators of neuronal pathfinding and angiogenesis. In the neuro-retinal tissue of the retina, semaphorins exert important functional roles on tissue homeostasis and architecture by guiding axons and vessels to their appropriate target and steering them away from unwanted compartments.

Methods and results: Using RNA and protein expression analysis on murine and human retinas, we identified Semaphorin 3F (Sema3F) to be expressed exclusively in the avascular layers of the outer retina (outer nuclear layer and retinal pigment epithelium; RPE). Using functional in vitro models, we found potent anti-angiogenic effects of Sema3F on human retinal endothelial cells in a spheroid assay as well as on choroidal endothelial cells in a choroidal explant assay. In addition, Sema3F expression in human RPE from active CNV membranes revealed a reduced expression of Sema3F in CNVRPE compared to normal RPE.

Conclusion: Our data demonstrate an exclusive expression of antiangiogenic Sema3F in the outer retinal layers. Physiologically, Sema3F may contribute to the avascularity of these retinal layers. In pathologic conditions like exudative AMD, reduced Sema3F expression may contibute to invasion of blood vessels into these normally avascular outer retinal layers.