Project description:To study early and late transcriptional changes introduced to blood and retinal tissue in murine oxygen-induced retinopathy (OIR). From blood MNCs total RNA was extracted at three time points: immediately after end of hyperoxia (P12), at P17 and P28.
Project description:To study early and late transcriptional changes introduced to blood and retinal tissue in murine oxygen-induced retinopathy (OIR). From retinal cells RNA was extracted at three time points: immediately after end of hyperoxia (P12), at P17 and P28.
Project description:High-throughput sequencing of murine retina of the oxygen induced retinopathy (OIR) model compared to control mice at 5 consecutive days (P12-P16)
Project description:Analysis of gene expression changes in oxygen-induced retinopathy mice treated intravitreally with inhibitors. oxygen-induced retinopathy(OIR)mice is one of the experimental systems that mimic retinal ischemic diseases. This model is widely used as an evaluation system for various surgical procedures.
Project description:To investigate the expression profile of genes involved in oxygen-induced retinopathy (OIR) and the effect of caspase1 deletion on those genes in retina.
Project description:Using Next Generation Sequencing (NGS) we profiled miRNA expression in the retina and choroid during degenerative and NV phases of oxygen-induced retinopathy (OIR).
Project description:Pathologic ocular angiogenesis is a common cause of blindness in proliferative retinopathy. Small non-coding RNAs (sncRNAs) play critical roles in normal development and diseases, and their function in eye diseases and angiogenesis are increasingly recognized. In the present study, we aimed to identify the function and therapeutic potential of sncRNAs in retinopathy. We used microarray to analyze the retinal expression profile of sncRNAs in a mouse oxygen-induced retinopathy (OIR) model that mimic human proliferative retinopathy.
Project description:Schemic retinopathies such as diabetic retinopathy (DR) and retinopathy of prematurity (ROP), are the main causes of blindness in working age and pediatric populations in industrialized countries. It is estimated that close to 100 million individuals worldwide suffer from DR and 15 million preterm infants born each year are predisposed to ROP. Regrettably, relatively little is known of the cellular processes at play during late stages of pathological angiogenesis in these diseases and consequently current standards of care target all neovascularization. Oxygen-induced retinopathy (OIR) allows to reproduce experimentally in the mouse retina the pathological features observed in human pathological retina such as ischemic avascular regions as well as epi-retinal neovascularization. Using agnostic and orthogonal approaches, in our work we demonstrate that in contrast to healthy blood vessels, pathological vessels engage pathways of cell cycle arrest, resulting in cellular senescence. These findings combined with further genetic and pharmacological approaches provide mechanistic evidence supporting that targeting selectively senescent vessels in DR represents a potential treatment for neovascular retinal disease.