Mouse iPS cells-derived 3D-retinas: Vehicle control- vs. 4-hydroxytamoxifen (4-OHT)-treated 3D-retinas
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE83985 | GEO | 2016/07/05
SECONDARY ACCESSION(S): PRJNA327747
REPOSITORIES: GEO
Similar Datasets
Project description:Transcriptional profiling of 3D-retinas differentiated from mouse iPS cells comparing vehicle control- with 4-OHT-treated. 4-OHT is an inverse agonist of estrogen-related receptor beta (ERRβ), a rod-enriched transcription factor responsible for maintenance of rod photoreceptor cells and the treatment induces photoreceptor specific cell death in the 3D-retinas. Goal was to understand the mechanism of 4-OHT-induced degeneration of photoreceptor cells in the 3D-retinas. 4-OHT-induced gene expression in the 3D-retinas was measured at DD 26 when the photoreceptor cells were degenerated. Two-condition experiment, vehicle control- vs. 5 µM 4-OHT-treated 3D-retinas. Biological replicates: each sample has 24 3D-retinas and 1 replicate.
2016-07-05 | E-GEOD-83985 | biostudies-arrayexpress
Project description:Transcriptional profiling of 3D-retinas differentiated from mouse iPS cells comparing vehicle control with 4-OHT-treated w/o supplements. 4-OHT is an inverse agonist of estrogen-related receptor beta (ERRβ), a rod-enriched transcription factor responsible for maintenance of rod photoreceptor cells and the treatment induces photoreceptor specific cell death in the 3D-retinas. Goal was to understand the mechanism of protective effects of representative ophthalmic supplements for treating the photoreceptor degeneration. 4-OHT w/o supplements-induced gene expression in the 3D-retinas was measured at DD 25 when the photoreceptor cells started to be degenerated. Four-condition experiment, vehicle control- vs. 5 µM 4-OHT- vs. 5 µM 4-OHT with 400 µM vitamin E- vs. 5 µM 4-OHT with 200 nM lutein-treated 3D-retinas. Biological replicates: each sample has 24 3D-retinas and 1replicate.
2016-07-05 | E-GEOD-83984 | biostudies-arrayexpress
Project description:Transcriptional profiling of 3D-retinas differentiated from mouse iPS cells comparing vehicle control with 4-OHT-treated w/o supplements. 4-OHT is an inverse agonist of estrogen-related receptor beta (ERRβ), a rod-enriched transcription factor responsible for maintenance of rod photoreceptor cells and the treatment induces photoreceptor specific cell death in the 3D-retinas. Goal was to understand the mechanism of protective effects of representative ophthalmic supplements for treating the photoreceptor degeneration.
2016-07-05 | GSE83984 | GEO
Project description:Mouse iPS cells-derived 3D-retinas
| PRJNA327746 | ENA
Project description:Purpose: Study the temporal effect of OHT on gene expression in MCF7 cells using mRNA-seq. Methods: MCF7 cells were treated with 100nM OHT for 2h, 6h and 24h or 24h with vehicle alone (ethanol). Six biological replicates of each time point were included in the analysis. For the library preparation the Illumina TruSeq Stranded mRNA Library Prep Kit High Throughput was used and 2 lanes of SE50 were run on HiSeq 4000. Results: We identify 27,520 genes of which 1,187 were significantly regulated in response to OHT in at least one time point. This included transcriptional repression of cell cycle genes as well as a number of known ERα target genes. Conclusions: We demonstrate a transcriptional response to OHT in MCF7 cells, with ERa target genes and genes linked to cell cycle progression being repressed.
2018-10-12 | GSE104872 | GEO
Project description:Neuronal plasticity of the inner retina has been observed in response to photoreceptor degeneration. Typically, this phenomenon has been considered maladaptive and may preclude vision restoration in the blind. However, several recent studies utilizing triggered photoreceptor ablation have shown adaptive responses in bipolar cell dendrites expected to support normal vision. Whether such homeostatic plasticity occurs during progressive photoreceptor degenerative disease to help maintain normal visual behavior is unknown. We addressed these issues in an established mouse model of Retinitis Pigmentosa caused by the P23H mutation in rhodopsin. We show robust modulation of the retinal transcriptomic network reminiscent of the neurodevelopmental state as well as potentiation of rod – rod bipolar cell signaling following rod photoreceptor degeneration. Additionally, we found highly sensitive night vision in P23H mice even when more than half of the rod photoreceptors were lost. The results implicate retinal adaptation leading to persistent visual function during photoreceptor degenerative disease.
2020-06-16 | GSE152474 | GEO
Project description:Neuronal plasticity of the inner retina has been observed in response to photoreceptor degeneration. Typically, this phenomenon has been considered maladaptive and may preclude vision restoration in the blind. However, several recent studies utilizing triggered photoreceptor ablation have shown adaptive responses in bipolar cell dendrites expected to support normal vision. Whether such homeostatic plasticity occurs during progressive photoreceptor degenerative disease to help maintain normal visual behavior is unknown. We addressed these issues in an established mouse model of Retinitis Pigmentosa caused by the P23H mutation in rhodopsin. We show robust modulation of the retinal transcriptomic network reminiscent of the neurodevelopmental state as well as potentiation of rod – rod bipolar cell signaling following rod photoreceptor degeneration. Additionally, we found highly sensitive night vision in P23H mice even when more than half of the rod photoreceptors were lost. The results implicate retinal adaptation leading to persistent visual function during photoreceptor degenerative disease.
2020-08-21 | GSE156533 | GEO
Project description:Photoreceptor disorders are collectively known as retinal degeneration (RD), and include retinitis pigmentosa (RP), cone-rod dystrophy and age related macular degeneration (AMD). These disorders are largely genetic in origin; individual mutations in any one of >200 genes cause RD, making mutation specific therapies prohibitively expensive. A better treatment plan, particularly for late stage disease, may involve stem cell transplants into the photoreceptor or ganglion cell layers of the retina. Stem cells from young mouse retinas can be transplanted, and can form photoreceptors in adult retinas. These cells can be grown in tissue culture, but can no longer form photoreceptors. We have used microarrays to investigate differences in gene expression between cultured retinal progenitor cells (RPCs) that have lost photoreceptor potential, postnatal day 1 (pn1) retinas and the postnatal day 5 (pn5) retinas that contain transplantable photoreceptors. We have also compared FACS sorted Rho-eGFP expressing rod photoreceptors from pn5 retinas with Rho-eGFP negative cells from the same retinas. We have identified over 300 genes upregulated in rod photoreceptor development in multiple comparisons, 37 of which have been previously identified as causative of retinal disease when mutated. It is anticipated that this research should bring us closer to growing photoreceptors in culture and therefore better treatments for RD. This dataset is also a resource for those seeking to identify novel retinopathy genes in RD patients. We extracted whole retinas from postnatal day 1 (Pn1) and postnatal day 5 (Pn5) mice, and compared them with cultured RPCs derived from pn5 retinas, using Affymetrix mouse 430A_2 arrays. We also extracted cells from Rho-eGFP Pn5 retinas and FACS sorted them. GFP+ve cells represent immature rod photoreceptors, as they express the Rho-eGFP fusion protein, which is only expressed in rods. GFP-ve cells represent all other retinal neurons. These samples were amplified and compared using Affymetrix mouse 430A_2arrays, by Source Biosciences GMBH, Berlin, Germany. Results from immature rods were then compared with those from other retinal neurons, while results from whole Pn5 retinas were compared with Pn1 retinas (which don't yet express rod specific genes), and RPCs, which are glial precursors. RPCs were also compared with Pn1 retinas. Genes which showed changed expression profiles in at least 3/4 of comparisons were prioritised for further investigation.
2015-01-20 | E-GEOD-59201 | biostudies-arrayexpress
Project description:To isolate photoreceptor precursors fit for transplantation, we adapted a 3D differentiation protocol that generates neuroretina from mouse ES cells. We used an adeno-associated viral vector (pseudotype2/9)carrying a GFP reporter under the control of a Rhodopsin promoter (AAV2/9.Rhop.GFP)to select rod precursors. AAV2/9.Rhop.GFP+ rods were sorted at days 26 and 34 and post natal day P12.
2013-07-17 | E-MEXP-3921 | biostudies-arrayexpress
Project description:Mutation of rod photoreceptor-enriched transcription factors is a major cause of inherited blindness. We identified the orphan nuclear hormone receptor ERRβ as selectively expressed in rod photoreceptors. Overexpression of ERRβ induces expression of rod-specific genes in retinas of both wildtype and in Nrl-/- mice, which lack rod photoreceptors. Mutation of ERRβ results in dysfunction and degeneration of rods, while inverse agonists of ERRβ trigger rapid rod degeneration, which is rescued by constitutively active mutants of ERRβ. ERRβ coordinates expression of multiple genes that are rate-limiting regulators of ATP generation and consumption in photoreceptors. Furthermore, enhancing ERRβ activity rescues photoreceptor defects that result from loss of the photoreceptor-specific transcription factor Crx. Our findings demonstrate that ERRβ is a critical regulator of rod photoreceptor function and survival, and suggest that ERRβ agonists may be useful in the treatment of certain retinal dystrophies. Affymetrix MOE430 microarrays were used to analyze the expression patterns of P21 mouse retinal tissues. The results were compared across the variable of Genotype, specifically ERRβ knockout versus wildtype.
2010-07-30 | E-GEOD-21944 | biostudies-arrayexpress