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: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: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: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.
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: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:<p>The retina is a notable tissue with high metabolic needs which relies on specialized vascular networks to protect the neural retina while maintaining constant supplies of oxygen, nutrients and dietary essential fatty acids. Here we analyzed the lipidome of the mouse retina under healthy and pathological angiogenesis using the oxygen-induced retinopathy model. By matching lipid profiles to changes in mRNA transcriptome, we identified a lipid signature showing that pathological angiogenesis leads to intense lipid remodeling favoring pathways for neutral lipid synthesis, cholesterol import/export and lipid droplet formation. Noteworthy, it also shows profound changes in pathways for long-chain fatty acid production, vital for retina homeostasis. The net result is accumulation of large quantities of mead acid, a marker of essential fatty acid deficiency, and a potential marker for retinopathy severity. Thus, our lipid signature might contribute to better understand diseases of the retina that lead to vision impairment or blindness.</p>