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24th Annual Meeting of the German Retina Society

German Retina Society

17.06. - 18.06.2011, Aachen

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DDAH-2 deletion promotes vascular regeneration in retinal ischemia

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  • Clemens Lange - Department of Genetics, Institute of Ophthalmology, UCL, London, UK
  • F. Mowat - Department of Genetics, Institute of Ophthalmology, UCL, London, UK
  • U.F.O. Luhmann - Department of Genetics, Institute of Ophthalmology, UCL, London, UK
  • H. Sayed - Department of Genetics, Institute of Ophthalmology, UCL, London, UK
  • P. Kelly - The British Heart Foundation Laboratories, Division of Medicine, UCL, London, UK
  • A.J. Smith - Department of Genetics, Institute of Ophthalmology, UCL, London, UK
  • J. Leiper - The British Heart Foundation Laboratories, Division of Medicine, UCL, London, UK
  • R.R. Ali - Department of Genetics, Institute of Ophthalmology, UCL, London, UK
  • J. Bainbridge - Department of Genetics, Institute of Ophthalmology, UCL, London, UK

German Retina Society. 24th Annual Conference of the German Retina Society. Aachen, 17.-18.06.2011. Düsseldorf: German Medical Science GMS Publishing House; 2011. Doc11rg52

doi: 10.3205/11rg52, urn:nbn:de:0183-11rg523

This is the English version of the article.
The German version can be found at: http://www.egms.de/de/meetings/rg2011/11rg52.shtml

Published: June 15, 2011

© 2011 Lange 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

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Background: Retinal ischemia and pathological angiogenesis is a central feature of common blinding disorders including retinal vascular occlusive disease and diabetic retinopathy. Dimethylarginine dimethylaminohydrolase 2 (DDAH2) is a key regulator of nitric oxide synthases and nitric oxide (NO) production. The aim of this study was to investigate the role of DDAH2 in physiological and pathological angiogenesis in the retina and choroid.

Methods: We assessed the vascular phenotype of DDAH2-knockout mice by in vivo fluorescein angiography and by immuno-histochemistry, and the retinal function by electroretinogram. We investigated the role of DDAH2 in pathological retinal and choroidal angiogenesis using the oxygen-induced retinopathy (OIR) and the laser-induced choroidal neovascularisation mouse model.

Results: DDAH2 deletion had no evident effect on normal retinal vasculature nor on retinal function. In the OIR model we found a significant reduction of the ischemic fraction (p<0.0001) and the preretinal pathological neovascularisation in DDAH2 deficient mice compared with wild type littermates (p<0.0001). We observed no significant difference in laser induced choroidal neovascularisation in DDAH2 deficient mice compared with wild type controls (p=0.17).

Conclusion: DDAH2 has an important role in retinal vascular repair and in the development of ischaemia-induced retinal neovascularisation. These results suggest that inhibition of DDAH-2 may offer a safe and efficient therapeutic strategy for retinal ischemia and pathological retinal neovascularisation.