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Expressional alterations of apoptosis-related genes after retinal ischemia with brimonidine pre-treatment
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Neuroscience, Developmental Neuroscience.
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Manuscript (Other academic)
URN: urn:nbn:se:uu:diva-97697OAI: oai:DiVA.org:uu-97697DiVA: diva2:172736
Available from: 2008-11-06 Created: 2008-11-06 Last updated: 2010-01-13Bibliographically approved
In thesis
1. Experimental Injury to the Visual System: Molecular Studies of the Retina
Open this publication in new window or tab >>Experimental Injury to the Visual System: Molecular Studies of the Retina
2008 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Retinal ganglion cells play a crucial role in the relay of visual signals from the eye to the brain. This cell type is affected and eventually lost in the eye disease glaucoma, resulting in progressive and irreversible loss of vision. Studies of the molecular mechanisms leading to retinal ganglion cell death are important for the understanding of the disease and for designing future treatments. This thesis addresses and studies these molecular mechanisms, including alterations in gene expression after experimental retinal injuries. The effects of a neuroprotective drug, brimonidine, after transient retinal ischemia were also studied in order to help explain the mechanisms behind the protective properties of this drug.

Several methods, including quantitative reverse transcriptase PCR, micro-arrays, western blot and immunohistochemistry, were used. The results showed that transient retinal ischemia triggers cell division in Müller cells and alters the gene expression of growth factors, their receptors, and intermediate filaments in the retina. Several genes related to the apoptosis process were less affected. Pre-treatment with brimonidine increased the levels of certain growth factors (BDNF, NT3, CNTF, FGF9) compared with vehicle. Brimonidine also had marked effects on genes related to progenitor cells, among them the recognized neural stem cell marker nestin. The increase in levels of nestin after ischemia was countered by brimonidine treatment. Moreover, retinal ganglion cell death following either optic nerve transection or optic nerve crush appears to involve the extrinsic apoptotic pathway although the gene expression response appears to differ between these injuries.

The results obtained in this work contribute to an increased understanding of retinal injuries and highlight the importance of Müller cells in the endogenous defense against retinal injuries.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2008. 61 p.
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 392
retina, injury, ischemia, gene expression, brimonidine, alpha-2-adrenergic agonist, neuroprotection, growth factors, apoptosis, Müller cells
National Category
urn:nbn:se:uu:diva-9344 (URN)978-91-554-7321-1 (ISBN)
Public defence
2008-11-28, B21, BMC, Husargatan 3, Uppsala, 09:15
Available from: 2008-11-06 Created: 2008-11-06Bibliographically approved

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