Feng, Yuxi; vom Hagen, Franziska; Pfister, Frederick; Djokic, Snezana; Hoffmann, Sigrid; Back, Walter; Wagner, Patrick; Lin, Jihong; Deutsch, Urban; Hammes, Hans-Peter (2007). Impaired pericyte recruitment and abnormal retinal angiogenesis as a result of angiopoietin-2 overexpression. Thrombosis and haemostasis, 97(1), pp. 99-108. Stuttgart: Schattauer 10.1160/TH06-05-0277
Full text not available from this repository.Angiopoietin-2 (Ang2) is among the relevant growth factors induced by hypoxia and plays an important role in the initiation of retinal neovascularizations. Ang2 is also involved in incipient diabetic retinopathy, as it may cause pericyte loss. To investigate the impact of Ang2 on developmental and hypoxia-induced angiogenesis, we used a transgenic mouse line overexpressing human Ang2 in the mouse retina. Transgenic mice displayed a reduced coverage of capillaries with pericytes (-14%; p < 0.01) and a 46% increase of vascular density of the capillary network at postnatal day 10 compared to wild type mice. In the model of oxygen-induced retinopathy (OIR), Ang2 overexpression resulted in enhanced preretinal (+103%) and intraretinal neovascularization (+29%). Newly formed intraretinal vessels in OIR were also pericyte-deficient (-26%; p < 0.01). The total expression of Ang2 in transgenic mice was seven-fold, compared with wild type controls. Ang2 modulated expression of genes encoding VEGF (+65%) and Ang1 (+79%) in transgenic animals. These data suggest that Ang2 is involved in pericyte recruitment, and modulates intraretinal, and preretinal vessel formation in the eye under physiological and pathological conditions.
Item Type: |
Journal Article (Original Article) |
---|---|
Division/Institute: |
04 Faculty of Medicine > Pre-clinic Human Medicine > Theodor Kocher Institute |
UniBE Contributor: |
Deutsch, Urban |
ISSN: |
0340-6245 |
ISBN: |
17200776 |
Publisher: |
Schattauer |
Language: |
English |
Submitter: |
Factscience Import |
Date Deposited: |
04 Oct 2013 14:52 |
Last Modified: |
05 Dec 2022 14:16 |
Publisher DOI: |
10.1160/TH06-05-0277 |
PubMed ID: |
17200776 |
Web of Science ID: |
000243432100017 |
URI: |
https://boris.unibe.ch/id/eprint/22210 (FactScience: 32274) |