gms | German Medical Science

102. Jahrestagung der DOG

Deutsche Ophthalmologische Gesellschaft e. V.

23. bis 26.09.2004, Berlin

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Retinal endothelial angiogenic activity: effects of hypoxia and glial (Müller) cells

Meeting Abstract

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  • corresponding author Y. Yafai - University of Leipzig, Eye Hospital, Leipzig
  • I. Iandiev - University of Leipzig, Paul Flechsig Institute of Brain Research, Department of Neurophysiology, Leipzig
  • P. Wiedemann - University of Leipzig, Eye Hospital, Leipzig
  • A. Reichenbach - University of Leipzig, Paul Flechsig Institute of Brain Research, Department of Neurophysiology, Leipzig
  • W. Eichler - University of Leipzig, Eye Hospital, Leipzig

Evidenzbasierte Medizin - Anspruch und Wirklichkeit. 102. Jahrestagung der Deutschen Ophthalmologischen Gesellschaft. Berlin, 23.-26.09.2004. Düsseldorf, Köln: German Medical Science; 2004. Doc04dogP 133

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dog2004/04dog624.shtml

Published: September 22, 2004

© 2004 Yafai et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

Outline

Text

Objective

To explore neovascularization-related activities of cultured retinal endothelial cells in response to hypoxia, and their modulation by retinal glial (Müller) cells.

Methods

Bovine retinal endothelial cells (BRECs) were cultured under normoxia or hypoxia (0.5% O2) either alone, together with the human Müller cell line MIO-M1, or in normoxia- or hypoxia-conditioned media of MIO-M1 cells. Cell number, proliferation, apoptotic cell death, and migration of BRECs were determined.

Results

Exposure of BRECs to hypoxia for 24 h decreased the number of adherent cells and the proliferation rate but increased apoptosis and cell migration. Increased apoptosis of the BRECs occured also in the presence of conditioned media of MIO-M1 cells but not during co-culture with MIO-M1 cells. Under normoxic conditions, co-culture resulted in increased proliferation, but decreased the migration rates of BRECs. Under hypoxia, the presence of Müller cells decreased the proliferation and migration rates of BRECs.

Conclusions

Hypoxia inhibits the proliferation of retinal endothelial cells. Müller cells release soluble mediators that enhance this hypoxia-mediated effect but, under certain conditions (i.e., in co-culture), may protect retinal endothelial cells from apoptosis, thus supporting their survival. Whereas the key signal(s) necessary to trigger retinal endothelial proliferation under hypoxia remain(s) to be determined, our observations indicate that Müller cells may be effective in preventing retinal neovascularization.