title: ICAM-1 depletion does not alter retinal vascular development in a model of oxygen-mediated neovascularization.
abstract: ICAM-1 has been identified as a mediator of inflammatory and VEGF-dependent corneal neovascularization. Furthermore, ICAM-1 has been demonstrated to be involved in leukocyte-mediated endothelial injury in diabetic retinopathy. Here we investigated the role of ICAM-1 in retinal vaso-obliteration and vascularization. ICAM-1 deficient mice as well as their respective wild-type controls were exposed to 75% oxygen from postnatal day 7 to day 12. Retinal vascularization was investigated after lectin labeling of endothelial cells on day 14, 17, and 20 in flat mount preparations. Retinal mRNA expression of VEGF, Angiopoietin 1 and 2 as well as PDGFbeta was examined at day 14 and 20 by Real Time RT-PCR. ICAM-1(-/-) mice and their respective wild-type controls demonstrated similar retinal development and vascularization under normoxic conditions. Similarly, after oxygen challenge, the vascular area, the avascularized area as well as the area of neovascular tufts did not differ between ICAM-1(-/-) and the respective wild-type mice although the mRNA expression of VEGF, ang-1, ang-2, and PDGFbeta differed clearly. This study demonstrates that lack of ICAM-1 leads to an altered expression of angiogenic factors that in combination may neutralize each other and do not alter retinal development and angiogenesis in oxygen-induced retinopathy.
authors.affiliation: Department of Ophthalmology, Heinrich-Heine University, Moorenstrasse 5, 40225 Duesseldorf, Germany. joussena@googlemail.com
authors.forename: Norbert
authors.initials: N
authors.lastname: Kociok
authors.forename: Sven
authors.initials: S
authors.lastname: Radetzky
authors.forename: Tim U
authors.initials: TU
authors.lastname: Krohne
authors.forename: Claudia
authors.initials: C
authors.lastname: Gavranic
authors.forename: Yong
authors.initials: Y
authors.lastname: Liang
authors.forename: Irina
authors.initials: I
authors.lastname: Semkova
authors.forename: Antonia M
authors.initials: AM
authors.lastname: Joussen
mesh_terms: D042683:Angiopoietin-1 / Q000235:genetics; D042702:Angiopoietin-2 / Q000235:genetics; D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D000860:Hypoxia / Q000378:metabolism; D007231:Infant, Newborn; D018799:Intercellular Adhesion Molecule-1 / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010100:Oxygen / Q000633:toxicity; D020574:Proto-Oncogene Proteins c-sis / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D015861:Retinal Neovascularization / Q000378:metabolism* / Q000473:pathology; D012171:Retinal Vessels / Q000378:metabolism* / Q000473:pathology; D012178:Retinopathy of Prematurity / Q000378:metabolism* / Q000473:pathology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics
chemical_list: D042683:Angiopoietin-1; D042702:Angiopoietin-2; C467628:Angpt1 protein, mouse; C090509:Icam1 protein, mouse; D020574:Proto-Oncogene Proteins c-sis; D012333:RNA, Messenger; D042461:Vascular Endothelial Growth Factor A; C467480:vascular endothelial growth factor A, mouse; D018799:Intercellular Adhesion Molecule-1; D010100:Oxygen