Mus musculus
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ABSTRACT:
PROVIDER: PRJNA215220 | ENA |
REPOSITORIES: ENA
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Project description:PURPOSE To identify retinal pigment epithelial (RPE)/choroid genes and their relevant expression pathways affected by intravitreal injections of dexamethasone and triamcinolone acetonide in mice at clinically relevant time points for patient care. METHODS Differential gene expression of over 34,000 well-characterized mouse genes, in the RPE/choroid of 6 week old C57BL/6J mice were analyzed after intravitreal steroid injections at 1 week and 1 month post injection, using Affymetrix Mouse Genome 430 2.0 microarrays. The data were analyzed using GeneSpringGX12.5 and Ingenuity Pathway Analysis (IPA) microarray analysis software for biologically relevant changes. RESULTS Both triamcinolone and dexamethasone caused differential activation of genes involved in âCircadian Rhythm Signalingâ pathway at both time points tested. Triamcinolone (TAA) uniquely induced significant changes in gene expression in âCalcium Signalingâ (1 week) and âGlutamate Signalingâ pathways (1month). In contrast, Dexamethasone (Dex) affected the âGABA Receptor Signalingâ (1 week) and âSerotonin Receptor Signalingâ (1month) pathways. CONCLUSIONS Understanding how intraocular steroids affect the gene expression of RPE/choroid is clinically relevant. This in vivo study has elucidated several genes and pathways that are potentially altering the circadian rhythms and several other neurotransmitter pathways in RPE/choroid cells during intravitreal steroid injections, which likely has consequences in the dysregulation of RPE function and neurodegeneration of the retina. Total of 18 RPE/choroid samples were analysed. There were two time points, day7 and day30. Each time point had three groups: BSS control, DEX treatment and TAA treatment. Each group had three biological replicas.
2016-08-01 | E-GEOD-49872 | biostudies-arrayexpress
Project description:PURPOSE To identify retinal pigment epithelial (RPE)/choroid genes and their relevant expression pathways affected by intravitreal injections of dexamethasone and triamcinolone acetonide in mice at clinically relevant time points for patient care. METHODS Differential gene expression of over 34,000 well-characterized mouse genes, in the RPE/choroid of 6 week old C57BL/6J mice were analyzed after intravitreal steroid injections at 1 week and 1 month post injection, using Affymetrix Mouse Genome 430 2.0 microarrays. The data were analyzed using GeneSpringGX12.5 and Ingenuity Pathway Analysis (IPA) microarray analysis software for biologically relevant changes. RESULTS Both triamcinolone and dexamethasone caused differential activation of genes involved in ‘Circadian Rhythm Signaling’ pathway at both time points tested. Triamcinolone (TAA) uniquely induced significant changes in gene expression in ‘Calcium Signaling’ (1 week) and ‘Glutamate Signaling’ pathways (1month). In contrast, Dexamethasone (Dex) affected the ‘GABA Receptor Signaling’ (1 week) and ‘Serotonin Receptor Signaling’ (1month) pathways. CONCLUSIONS Understanding how intraocular steroids affect the gene expression of RPE/choroid is clinically relevant. This in vivo study has elucidated several genes and pathways that are potentially altering the circadian rhythms and several other neurotransmitter pathways in RPE/choroid cells during intravitreal steroid injections, which likely has consequences in the dysregulation of RPE function and neurodegeneration of the retina.
2016-08-01 | GSE49872 | GEO
Project description:PURPOSE To identify retinal genes and their relevant expression pathways affected by intravitreal injections of dexamethasone and triamcinolone acetonide in mice at clinically relevant time points for patient care. METHODS Differential gene expression of over 34,000 well-characterized mouse genes, in the retinas of 6 weeks old C57BL/6J mice were analyzed after intravitreal steroid injections at 1 week and 1 month time points, using Affymetrix Mouse Genome 430 2.0 microarrays. The data were analyzed using GeneSpringGX11 and Ingenuity Pathway Analysis (IPA) microarray analysis software for biologically relevant changes. RESULTS A common gene pathway, with differentially activated genes for both steroids and time points was ‘Semaphorin Signaling in Neurons’, a member of ‘Axonal Guidance Signaling System’. At 1 week post-injections a common theme was activation of genes expressed in retinal glial cells, TNF alpha and TGF beta signaling pathways and upregulation of stress response proteins (Serpina3n, Cebpd), as well as neuropeptide signaling somatostatin receptor (Sstr2). Unique for Dex was the upregulation of acute phase proteins (Gfap, Cp, Edn2) as well as Plexna2, a semaphorin signaling receptor, while EphrinB receptor ephexin1 (Argef15) was downregulated. Folate signaling appears to be unique for TAA at 1 week (Folh1, Cubn), while aryl-hydrocarbon receptor (AhR) signaling might be important for both steroids at 1 month. CONCLUSIONS Understanding the molecular and genetic effects of intraocular steroid treatments is of clinical relevance. This in vivo study has elucidated several genes and pathways that are potentially altering the neuroprotective/neurodegenerative balance between glial and retinal ganglion cells during intravitreal steroid treatment. Total of 18 retinal samples were analysed. There were two time points, day7 and day30. Each time point had three groups: BSS control, DEX treatment and TAA treatment. Each group had three biological replicas.
2011-12-08 | E-GEOD-30701 | biostudies-arrayexpress
Project description:In vivo Gene Expression Profiling of Retina Post-Intravitreal Injections of Dexamethasone and Triamcinolone at Clinically Relevant Time Points for Patient Care
| PRJNA144359 | ENA
Project description:PURPOSE To identify retinal genes and their relevant expression pathways affected by intravitreal injections of dexamethasone and triamcinolone acetonide in mice at clinically relevant time points for patient care. METHODS Differential gene expression of over 34,000 well-characterized mouse genes, in the retinas of 6 weeks old C57BL/6J mice were analyzed after intravitreal steroid injections at 1 week and 1 month time points, using Affymetrix Mouse Genome 430 2.0 microarrays. The data were analyzed using GeneSpringGX11 and Ingenuity Pathway Analysis (IPA) microarray analysis software for biologically relevant changes. RESULTS A common gene pathway, with differentially activated genes for both steroids and time points was ‘Semaphorin Signaling in Neurons’, a member of ‘Axonal Guidance Signaling System’. At 1 week post-injections a common theme was activation of genes expressed in retinal glial cells, TNF alpha and TGF beta signaling pathways and upregulation of stress response proteins (Serpina3n, Cebpd), as well as neuropeptide signaling somatostatin receptor (Sstr2). Unique for Dex was the upregulation of acute phase proteins (Gfap, Cp, Edn2) as well as Plexna2, a semaphorin signaling receptor, while EphrinB receptor ephexin1 (Argef15) was downregulated. Folate signaling appears to be unique for TAA at 1 week (Folh1, Cubn), while aryl-hydrocarbon receptor (AhR) signaling might be important for both steroids at 1 month. CONCLUSIONS Understanding the molecular and genetic effects of intraocular steroid treatments is of clinical relevance. This in vivo study has elucidated several genes and pathways that are potentially altering the neuroprotective/neurodegenerative balance between glial and retinal ganglion cells during intravitreal steroid treatment.
2011-12-08 | GSE30701 | GEO
Project description:To characterize underlying changes in the retinal pigment epithelium (RPE)/choroid with age, we produced gene expression profiles for the RPE/choroid and compared the transcriptional profiles of the RPE/choroid from young and old mice. The changes in the aged RPE/choroid suggest that the tissue has become immunologically active. Such phenotypic changes in the normal aged RPE/choroid may provide a background for the development of age-related macular degeneration. Experiment Overall Design: We compared the gene expression of retinal pigmental epithelium/choroid from young and old animals. There were 4 samples from young mice and 4 samples from old mice. Each sample contained 4 retinal pigmental epithelium/choroid from 2 animals
2008-06-11 | E-GEOD-10965 | biostudies-arrayexpress
Project description:To characterize underlying changes in the retinal pigment epithelium (RPE)/choroid with age, we produced gene expression profiles for the RPE/choroid and compared the transcriptional profiles of the RPE/choroid from young and old mice. The changes in the aged RPE/choroid suggest that the tissue has become immunologically active. Such phenotypic changes in the normal aged RPE/choroid may provide a background for the development of age-related macular degeneration. Keywords: age-related change
2008-03-29 | GSE10965 | GEO
Project description:Wet age-related macular degeneration (AMD), characterized by leaky neovessels emanating from the choroid, is a main cause of blindness. As current treatments for wet AMD require regular intravitreal injections of anti-VEGF biologics, there is a need for the novel development of less invasive treatments. Here, we developed a novel inhibitor of microtubule-associated End Binding 3 protein (EB3), herein termed EBIN, which blocked pathological Ca2+ signaling in activated endothelial cells and suppressed leakage of choroidal neovessels. Delivery of EBIN via eye drops in mouse and non-human primate (NHP) models of AMD prevented neovascular leakage and neovascularization as effectively as intravitreal injection of anti-VEGF therapy. EBIN activated Meis2-Pax6 regenerative pathways in metabolic-active endothelial cells comprising neovessels and promoted tissue regeneration. Furthermore, single nuclei assay for transposase-accessible chromatin sequencing (sn-ATAC-seq) analysis demonstrated that in metabolic-active endothelial cells, the RPE, and photoreceptors, EBIN induced global increases in chromatin accessibility, the biological process progressively inhibited in AMD patients. These results suggest the unique therapeutic mode of action of this novel drug candidate, which can potentially promote regeneration of eye tissue by reversing the degenerative processes underlying both the neovascular and atrophic forms of AMD.
2023-08-30 | GSE228269 | GEO
Project description:Wet age-related macular degeneration (AMD), characterized by leaky neovessels emanating from the choroid, is a main cause of blindness. As current treatments for wet AMD require regular intravitreal injections of anti-VEGF biologics, there is a need for the novel development of less invasive treatments. Here, we developed a novel inhibitor of microtubule-associated End Binding 3 protein (EB3), herein termed EBIN, which blocked pathological Ca2+ signaling in activated endothelial cells and suppressed leakage of choroidal neovessels. Delivery of EBIN via eye drops in mouse and non-human primate (NHP) models of AMD prevented neovascular leakage and neovascularization as effectively as intravitreal injection of anti-VEGF therapy. EBIN activated Meis2-Pax6 regenerative pathways in metabolic-active endothelial cells comprising neovessels and promoted tissue regeneration. Furthermore, single nuclei assay for transposase-accessible chromatin sequencing (sn-ATAC-seq) analysis demonstrated that in metabolic-active endothelial cells, the RPE, and photoreceptors, EBIN induced global increases in chromatin accessibility, the biological process progressively inhibited in AMD patients. These results suggest the unique therapeutic mode of action of this novel drug candidate, which can potentially promote regeneration of eye tissue by reversing the degenerative processes underlying both the neovascular and atrophic forms of AMD.
2023-08-30 | GSE228273 | GEO
Project description:Wet age-related macular degeneration (AMD), characterized by leaky neovessels emanating from the choroid, is a main cause of blindness. As current treatments for wet AMD require regular intravitreal injections of anti-VEGF biologics, there is a need for the novel development of less invasive treatments. Here, we developed a novel inhibitor of microtubule-associated End Binding 3 protein (EB3), herein termed EBIN, which blocked pathological Ca2+ signaling in activated endothelial cells and suppressed leakage of choroidal neovessels. Delivery of EBIN via eye drops in mouse and non-human primate (NHP) models of AMD prevented neovascular leakage and neovascularization as effectively as intravitreal injection of anti-VEGF therapy. EBIN activated Meis2-Pax6 regenerative pathways in metabolic-active endothelial cells comprising neovessels and promoted tissue regeneration. Furthermore, single nuclei assay for transposase-accessible chromatin sequencing (sn-ATAC-seq) analysis demonstrated that in metabolic-active endothelial cells, the RPE, and photoreceptors, EBIN induced global increases in chromatin accessibility, the biological process progressively inhibited in AMD patients. These results suggest the unique therapeutic mode of action of this novel drug candidate, which can potentially promote regeneration of eye tissue by reversing the degenerative processes underlying both the neovascular and atrophic forms of AMD.
2023-08-30 | GSE228270 | GEO