gms | German Medical Science

102. Jahrestagung der DOG

Deutsche Ophthalmologische Gesellschaft e. V.

23. bis 26.09.2004, Berlin

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IGF-1 induced VEGF secretion by RPE cells from CNV membranes

Meeting Abstract

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  • corresponding author O. Strauß - Experimentelle Ophthalmologie, Universitätsklinikum Hamburg-Eppendorf
  • C. Bowes-Rickman - Ophthalmology, Duke University Medical Center, Durham
  • G. Malek - Ophthalmology, Duke University Medical Center, Durham
  • L. L. Hansen - Universitäts-Augenklinik Freiburg
  • G. Martin - Universitäts-Augenklinik Freiburg
  • G. Richard - Experimentelle Ophthalmologie, Universitätsklinikum Hamburg-Eppendorf
  • R. Rosenthal - Klinische Physiologie, Charite Campus Benjamin Franklin, Berlin

Evidenzbasierte Medizin - Anspruch und Wirklichkeit. 102. Jahrestagung der Deutschen Ophthalmologischen Gesellschaft. Berlin, 23.-26.09.2004. Düsseldorf, Köln: German Medical Science; 2004. Doc04dogP 056

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/dog2004/04dog547.shtml

Veröffentlicht: 22. September 2004

© 2004 Strauß 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

Objective

Recently, the abundance of insulin-like growth factor-1 (IGF-1) in choroidal neovascular (CNV) membranes from patients with age-related macular degeneration (AMD) has been reported. IGF-1 is known to be released in response to hypoxia and to stimulate secretion of vascular endothelial growth factor (VEGF). Purpose of the study is to clarify the role of IGF-1 in the pathogenesis of CNV in AMD.

Methods

CNV membranes removed after eye surgery of AMD patients were analysed by means of immune histology. RPE cells from CNV membranes were isolated and subjected for primary culture. VEGF secretion rate was measured using ELISA. Intracellular free Ca2+ was measured in cultured RPE cells from CNV membranes using the Ca2+ sensitive fluorescence dye fura-2.

Results

Freshly isolated CNV membranes showed extensive staining for IGF-1. Furthermore, RPE cells in CNV membranes expressed the IGF-1 receptor IGF-1R. Western-blot analysis of membrane proteins from cultured RPE cells from CNV membranes confirmed the expression of IGF-1R. Application of IGF-1 to RPE cells from CNV membranes leads to an increase in intracellular free Ca2+ as second-messenger. Cultured RPE cells from CNV membranes showed a basic secretion of VEGF which could be increased 2-fold by IGF-1 application.

Conclusions

The abundant expression of IGF-1 could be confirmed by our data. Furthermore, RPE cells in CNV membranes showed expression of the IGF-1 receptor in situ histology and western-blot. IGF-1 induced rises in cytosolic free Ca2+ as second-messenger in response to IGF-1 confirmed that IGF-1 receptor is functionally present and induced VEGF secretion by RPE cells from CNV membranes. Thus, IGF-1 plays an important role in the development of CNV by induction of VEGF secretion by RPE cells.