gms | German Medical Science

26. Jahrestagung der Deutschen Retinologischen Gesellschaft

Deutsche Gesellschaft für Retinologie

27.09.2013, Hamburg

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Inactivation of HIF1a and VEGFA in myeloid cells reduces retinal and choroidal neovascularisation

Meeting Abstract

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  • Clemens Lange - Department of Genetics, Institute of Ophthalmology, UCL, NIHR Biomedical Research Centre for Ophthalmology, London, UK; University Eye Hospital Freiburg, Germany
  • A. Fantin - Department of Cell Biology, UCL Institute of Ophthalmology, London, UK
  • L. Denti - Department of Cell Biology, UCL Institute of Ophthalmology, London, UK
  • A. J. Smith - Department of Genetics, Institute of Ophthalmology, UCL, NIHR Biomedical Research Centre for Ophthalmology, London, UK
  • R.R. Ali - Department of Genetics, Institute of Ophthalmology, UCL, NIHR Biomedical Research Centre for Ophthalmology, London, UK
  • C. Ruhrberg - Department of Cell Biology, UCL Institute of Ophthalmology, London, UK
  • J.W. Bainbridge - Department of Genetics, Institute of Ophthalmology, UCL, NIHR Biomedical Research Centre for Ophthalmology, London, UK

Retinologische Gesellschaft. 26. Jahrestagung der Retinologischen Gesellschaft. Hamburg, 27.-27.09.2013. Düsseldorf: German Medical Science GMS Publishing House; 2013. Doc13rg07

doi: 10.3205/13rg07, urn:nbn:de:0183-13rg073

Veröffentlicht: 20. August 2013

© 2013 Lange 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

Myeloid cells have been implicated in retinal and choroidal neovascularization in sight-threatening neovascular eye diseases such as diabetic retinopathy and age-related macular degeneration. The hypoxia-inducible transcription factor 1 alpha (HIF1A) is activated by inflammatory stimuli and hypoxia and is a key driver of vascular endothelial growth factor (VEGFA) gene expression. This study explores the role of HIF1a and VEGFA in the development of retinal neovascularisation (RNV) after oxygen-induced retinopathy (OIR) and choroidal neovascularisation (CNV) after laser injury of Bruch’s membrane in mice with defective HIF1A and VEGFA expression in myeloid cells. We show that myeloid cells accumulate in areas of RNV or CNV at the onset of neovascularization and that both HIF1a activation and VEGFA expression in myeloid cells contribute substantially to the development of retinal and choroidal neovascularisation. These findings provide novel insight into the pathogenic mechanisms of neovascular eye disease and raise the possibility that immunomodulation of myeloid cells may provide a therapeutic approach to inhibit pathological angiogenesis.