Altered Retinal Revascularisation in TNF Receptor-1 and ICAM-1-deficient Mice in Oxygen-induced Retinopathy
Krohne T. U., Radetzky S., Kociok N., Joussen A. M.
Abteilung für Netzhaut- und Glaskörperchirurgie, Zentrum für Augenheilkunde, Universität zu Köln
Purpose: Tumour necrosis factor alpha (TNFa) and intracellular adhaesion molecule 1 (ICAM-1) are mediators of inflammation that are involved in leukocyte adhaesion and endothelial cell apoptosis in diabetic retinopathy. Furthermore ICAM-1 plays a role as mediator of inflammatory and VEGF-dependent corneal neovascularisation. The current study investigates wether these molecules of inflammation also influence retinal neovascularisation.
Method: TNF receptor-1 (TNFR1) and ICAM-1 deficient mice as well as wildtype controls were exposed to 70% oxygen from postnatal day 7 to 12. At days 14, 17 and 20 the retinal vasculature was lectin-labeled and analysed in flat-mount preparations. Quantitative measurements were obtained for total vessel area, avascular area and neovascularisation area. In addition, VEGF mRNA expression was analysed at days 14 and 20 by quantitative real-time RT-PCR.
Results: Untreated TNFR1 and ICAM-1 deficient mice and wildtype mice exhibit similar retinal development and vascularisation. Following oxygen exposure TNFR1 deficient mice as well as ICAM-1 deficient mice demonstrate decreased revascularisation of the retina as compared with wildtype mice. In wildtype mice an significant increase in VEGF expresseion was detected after oxygen t
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