gms | German Medical Science

102. Jahrestagung der DOG

Deutsche Ophthalmologische Gesellschaft e. V.

23. bis 26.09.2004, Berlin

The effect of VEGF-C on secretion of VEGF-A of the RPE

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  • corresponding author J. Weißmann - Department of Ophthalmology, University-Hospital Hamburg
  • S. Ehmer - Department of Ophthalmology, University-Hospital Hamburg
  • O. Strauß - Department of Ophthalmology, University-Hospital Hamburg

Evidenzbasierte Medizin - Anspruch und Wirklichkeit. 102. Jahrestagung der Deutschen Ophthalmologischen Gesellschaft. Berlin, 23.-26.09.2004. Düsseldorf, Köln: German Medical Science; 2004. Doc04dogP 177

The electronic version of this article is the complete one and can be found online at:

Published: September 22, 2004

© 2004 Weißmann et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.




The Effect of VEGF-A on endothelial cells in the development of CNV is well described. RPE-cells are a main source for VEGF-A and express the receptors VEGFR-1 and VEGFR-2 as well. It has been reported that cells from excised CNV-Membranes show a higher expression of VEGFR-2. Purpose of this study is the analysis of possible autocrine "feed-back-loops" on the VEGF production by an increased secretion of VEGF from RPE-cells. These feed-back-loops may act as inducers of CNV.


VEGF-secretion was measured by the increase of concentration of VEGF in culture medium from 105 ARPE 19 cells. Concentration of VEGF was measured using a Sandwich ELISA.


After the last exchange of culture medium the concentration of VEGF increased continuously and reached a maximum of 295pg/ml after 8 hours. By adding the VEGF analogon VEGF-C this basal secretion could be elevated up to 127,5% of control. After 8 hours under these conditions the VEGF concentration reached 375pg/ml.


VEGF-C which has a high affinity to VEGF-R2 stimulates the secretion of VEGF-A in RPE-cells efficiently. Thus, the VEGF-C dependend control of the VEGF-A secretion of the RPE is another possible mechanism causing induction of CNV in AMD.