Hotelbuchung
Hotel Registration
Grußwort
Welcome address
Beteiligte Gesellschaften
Societies involved
DOG Information
DOG Information
Eröffnung des Kongresses
Opening Ceremony
Preise
Awards
Ablauf der Tagung 2003
General overview of congress
Lageplan der Räumlichkeiten
Map of Congress Center
Wissenschaftliche Themen
Scientific topics
Symposien
Symposia
Wissenschaftliches Programm
Scientific program
Posterpräsentationen
Poster Presentation
Kurse
Courses
Begleitende Veranstaltungen
Accompanying program
Arbeitssitzungen
Working sessions
Rahmenprogramm
Social program
Allgemeine Informationen
General Information
Autorenindex
Index of Authors
Industrieaussteller
Commercial exhibitors
Sponsoren
Sponsors
Impressum
DOG Homepage
Abstract
Abstract
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