Channelpedia

PubMed 21487926


Referenced in: none

Automatically associated channels: Kir4.1



Title: Effects of intravitreal triamcinolone acetonide on retinal gene expression in a rat model of central retinal vein occlusion.

Authors: Matus Rehak, Franziska Drechsler, Patricia Köferl, Margrit Hollborn, Peter Wiedemann, Andreas Bringmann, Leon Kohen

Journal, date & volume: Graefes Arch. Clin. Exp. Ophthalmol., 2011 Aug , 249, 1175-83

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/21487926


Abstract
The aim of this study was to investigate the effects of intravitreal triamcinolone acetonide on the alterations in retinal gene expression in a rat model of central retinal vein occlusion (CRVO).In one eye of adult Brown Norway rats (n = 77) CRVO was induced with laser photocoagulation of all retinal veins near to the optic disk after intraperitoneal injection of 0.2 ml of 10% sodium fluorescein. The gene expression was investigated using RT-PCR separately in the neural retina and retinal pigment epithelium (RPE) 1, 3, 7, and 14 days after CRVO induction. We analyzed the expression of factors that influence the development of vascular edema (VEGF-A, VEGF-B, PEDF), of channels implicated in retinal osmohomeostasis (Kir4.1, AQP4, AQP1), and of the pro-inflammatory factors IL-1ß and IL-6.CRVO induced a rapid transient upregulation of Vegfa, a downregulation of Vegfb, and a delayed upregulation of Pedf in the neuroretina. In the neuroretina and retinal pigment epithelium, CRVO induced strong, transient downregulation of Kir4.1, Aqp4, and Aqp1, and striking rapid upregulation of Il1ß and Il6. Intravitreal triamcinolone reversed the downregulation of Kir4.1 and accelerated the normalization of the upregulated expression of Il1ß and Il6. The CRVO-induced transient upregulation of Vegfa was not influenced by the triamcinolone application.Triamcinolone exerts anti-inflammatory effects in the ischemic retina by inhibitory effects on the gene expression of IL-1ß and IL-6, and may have neuroprotective effects via improvement of retinal potassium homeostasis.