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Increased intravitreal angiopoietin-2 levels associated with rhegmatogenous retinal detachment
Authors:Sirpa Loukovaara  Kaisa Lehti  Alexandra Robciuc  Timo Pessi  Juha M Holopainen  Katri Koli  Ilkka Immonen  Jorma Keski-Oja
Institution:1. Unit of Vitreoretinal Surgery, Department of Ophthalmology, Helsinki University Central Hospital, Haartmaninkatu 4 C, 00290, Helsinki, Finland
2. Genome-Scale Biology, Haartman Institute, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland
4. Helsinki Eye Laboratory, Department of Ophthalmology, University of Helsinki, Helsinki, Finland
5. National Institute of Health and Welfare, Institute for Molecular Medicine, Biomedicum Helsinki, Helsinki, Finland
6. Datawell Oy, Espoo, Finland
3. Molecular Cancer Biology, Haartman Institute, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland
Abstract:

Purpose

To explore factors related to pathogenesis of rhegmatogenous retinal detachment (RRD) and development of proliferative vitreoretinopathy (PVR), vitreous levels of angiopoietin-1 and ?2 (Ang-1 and ?2), previously undefined in RRD, transforming growth factor-(TGF) β1, vascular endothelial growth factor (VEGF), erythropoietin (EPO) and proteolytic mediators of extracellular matrix remodelling (MMP-2 and ?9) were compared in eyes with RRD and eyes with idiopathic macular hole or pucker.

Methods

Vitreous samples were collected from 117 eyes with RRD (study group) and 40 eyes with macular hole or pucker (control group). Growth factors were measured by ELISA and matrix metalloproteinases (MMPs) by gelatin zymography.

Results

The mean vitreous concentrations of Ang-2, MMP-2, and MMP-9 were higher (all p?<?0.01), whereas concentration of VEGF was lower (p?=?0.01) in eyes with RRD relative to controls. Logistic regression analysis identified Ang-2 concentration as a novel marker of RRD (p?=?0.0001, OR 48.7). Ang-1, EPO, and total TGF-β1 levels were not significantly different between the groups. However, TGF-β1 and MMP-2 were increased in eyes with total RRD compared to those with local RRD (p?≤?0.05). In eyes with PVR, no differences were observed in any studied marker as compared with non-PVR eyes.

Conclusions

Current results reveal Ang-2 as a key factor upregulated in RRD. It may co-operate with fibrosis-associated factors and contribute to vascular complications such as breakdown of blood–eye barrier and PVR development.
Keywords:
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