Project description:This study investigated the effect of the Gnat1 (rod transducin alpha subunit) gene deficiency in Gnat1rd17 mice on the retinal transcriptome remodeling, and whether this remodeling is protective or maladaptive with regard to photoreceptor damage driven by autoimmune process. The results of this study showed that Gnat1rd17 mice exhibited transcriptomic changes indicative of remodeling in photoreceptor segments and connecting cilium, deregulated inflammatory pathways and dopaminergic signaling, followed by development of exacerbated experimental autoimmune uveoretinitis, which was ameliorated by dopamine replacement. These findings suggest rod transducin alpha subunit a critical modulator of retinal homeostasis and immune response through regulation of retinal dopaminergic system.
Project description:We have used surgical specimens to perform a differential analysis of the transcriptome of human retinal tissues following detachment. Data analysis reveals major involvement of the immune response in the disease and interindividual variation was monitored to unravel a second crucial aspect of the pathological process, the death of photoreceptor cells. In total 38 surgical specimens (samples) were analyzed, 19 represent biopsies from patients with retinal detachment (RD) and 19 represent contral samples without retinal detachment.
Project description:Retinal detachment is a major cause of blindness due to penetrating trauma and ocular inflammation, and is often observed in many patients following cataract extraction surgery. When the retinal photoreceptors detach from their epithelium, stress signals and apoptotic pathways are initiated that will lead to loss of vision, however accelerating the reattachment of these cells can prevent photoreceptor death and subsequent vision loss. To determine the genes involved in this process, we performed a microarray screen using a mouse model or retinal detachment in conjunction with a P2Y2 agonist previously demonstrated to hasten retinal reattachment. Experiment Overall Design: We conducted a microarray screen to identify genes involved in promoting faster resolution of retinal detachment. Subretinal detachment was induced in Balb/cJ mice by subretinal injection of 1 uL saline or delivery of 1 uL of 10uM INS37217/Saline to cause detachment and expedite the rate of recovery. We performed this study at three timepoints: 2 hrs post-injection to identify early response genes; 24 hrs post-detachment when the retina has reattached, but still grossly misfolded; and 7 days post-detachment when the misfolding has been resolved, but retinal function is merely 50% of wild-type function. We used each RNA pool (each containing >5 retinas) for GeneChip hybridization giving a total of 3 biological replicates for each treatment at each timepoint. For each GeneChip, we labeled 7 ug of total RNA according to the manufacturerâs specifications (Affymetrix Inc.).
Project description:Retinal detachment is a major cause of blindness due to penetrating trauma and ocular inflammation, and is often observed in many patients following cataract extraction surgery. When the retinal photoreceptors detach from their epithelium, stress signals and apoptotic pathways are initiated that will lead to loss of vision, however accelerating the reattachment of these cells can prevent photoreceptor death and subsequent vision loss. To determine the genes involved in this process, we performed a microarray screen using a mouse model or retinal detachment in conjunction with a P2Y2 agonist previously demonstrated to hasten retinal reattachment. Keywords: disease state analysis and therapeutic analysis
Project description:We aimed to evaluate changes in expression in control and th1/th1 mice treated with PBS and apo-transferrin to understand the effect(s) of exogenous apo-transferrin on normal and ineffective erythropoiesis
Project description:HiSER, established in our laboratory, exhibits ocular abnormalities including opacity, lens involution, and retinal detachment. To identify a causative gene(s) of the HiSER phenotype, microarray analysis was performed between HiSER and normal (SDR) eyes.
Project description:HiSER, established in our laboratory, exhibits ocular abnormalities including opacity, lens involution, and retinal detachment. To identify a causative gene(s) of the HiSER phenotype, microarray analysis was performed between HiSER and normal (SDR) eyes. Total RNA was extracted from HiSER and normal (SDR) eyes, and subjected to microarray analysis.
