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Retinitis pigmentosa (RP) mouse cone transcriptom change with Txnip treatment

ABSTRACT: Purpose: To identifiy mRNA changes in retinitis pigmentosa (RP) cone photoreceptors with Txnip overexpression treatment, which improved RP cone survival and visual acuity. Methods: two RP mouse strains, rd1 and Rho-/-, were injected with AAV-Txnip or AAV-H2BGFP control subretinally at P0. Retinas were dissected out at P21 for rd1 and P90 for Rho-/-. 1,000 H2BGFP labeled cones per retina sample were FACS sorted out, and subject for RNA-sequencing. Results: >1,400 genes in P21 rd1 and >700 genes in Rho-/- were found differentially expressed with Txnip treatment. Conclusions: 25 genes are in common between P21 rd1 and P90 Rho-/- with Txnip treatment. On this list, notably, three mitochondrial Electron Transport Chain (ETC) genes were up-regulated.

ORGANISM(S): Mus musculus

PROVIDER: GSE161622 | GEO | 2021/01/20

REPOSITORIES: GEO

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Wildtype (wt) mouse cone transcriptome change with Txnip treatment

Project description:Purpose: To identifiy mRNA changes in wt cone photoreceptors with Txnip overexpression treatment, which improved retinitis pigmentosa (RP) cone survival and visual acuity. Methods: two wt mouse strains, BALB/c and C57BL/6J were injected with AAV-Txnip or AAV-H2BGFP control subretinally at P0. Retinas were dissected out at P21 for BALB/c and P35 for C57BL/6J. 1,000 H2BGFP labeled cones per retina sample were FACS sorted out, and subject for RNA-sequencing. Results: only ~70 genes in P21 BALB/c and 1 genes in C57BL/6J were found differentially expressed with Txnip treatment. Only 1 genes (i.e. Txnip) were in commonly upregulated between the two lists. Conclusions: Txnip seems to be not changing RNA expression much in wt cones. Instead, its major function to rescue RP cones may lay in protein-protein interactions.

2021-03-15 | GSE168503 | GEO

Retinitis pigmentosa (RP) mouse cone transcriptom change with Txnip treatment

Project description:Retinitis pigmentosa (RP) mouse cone transcriptom change with Txnip treatment

| PRJNA678960 | ENA

RNA-seq analysis to assess transcriptional effects of Rp mutations in wing imaginal discs and their dependence on Xrp1

Project description:Since the putative transcription factor Xrp1 gene is required for many aspects of Rp+/- phenotypes, we sought to define what transcriptional changes occur in Rp+/- wing discs and their dependence on Xrp1. We identified 257 genes whose transcripts were significantly altered in the same direction in two Rp+/- genotypes, most of which depended on Xrp1. The results show that Xrp1 regulates a significant transcriptional response in Rp+/- genotypes.

2018-08-20 | GSE112864 | GEO

Ifh1 activates RP genes

Project description:Experiment Design: •Type of experiment: time course after GAL (galactose) induction •Experimental factor: time, genotype •Number of hybridizations performed in the experiment: 24 (eight conditions with three biological replicates each) Samples used, extract preparation and labeling: •The origin of the biological sample: Species: S. cerevisiae Cell type: wild-type (YSS37, IFH1-13myc-TRP1, MATa) UASIFH1::HIS3-UASGAL1 (YSS89, UASGAL1-IFH1-13myc-TRP1, MATa) •Growth conditions: log phase (2x107/mL) at 30°C in YPLG medium, then addition of Galactose to 2% •Treatments: all cells were harvested by rapid centrifugation at 4°C then flash frozen in liquid nitrogen. Keywords = IFH1 Keywords = Transcriptional control of RP genes Keywords: time-course

2004-11-06 | GSE1934 | GEO

HDAC inhibition ameliorates cone survival in retinitis pigmentosa mice

Project description:Cone photoreceptor cell death in inherited retinal diseases, such as Retinitis Pigmentosa (RP), leads to the loss of accurate and color vision and ultimately blindness. In RP, a vast number of mutations are affecting the structure and function of rod photoreceptors while cones remain mutation-free. Once majority of rods have degenerated cones are dying secondarily due to the increased oxidative stress, inflammation and loss of structural and nutritional support normally provided by rods. Here we demonstrated that secondary cone cell death in animal models for RP is governed by an increased activity of histone deacetylates (HDACs). A single intravitreal injection of an HDAC inhibitor at a late stage of the disease, when majority of rods have already degenerated, is sufficient to delay cone death and support long-term cone survival. Surviving cones are retaining functionality and are mediating light-driven ganglion cell responses. RNA-seq analysis of surviving cones demonstrated that HDAC inhibition affords multi-level protection trough regulation of different prosurvival pathways including MAPK, PI3K-AKT and autophagy. These study suggest a unique possibility for targeted pharmacological protection of both primary degenerating rods and mutation-free secondary dying cones and creates hope to maintain vision in RP patients independent of the disease stage.

2020-11-04 | GSE141601 | GEO

GENE EXPRESSION CHANGES WITHIN MÜLLER GLIAL CELLS DURING RETINITIS PIGMENTOSA

Project description:Retinitis Pigmentosa (RP) is a progressive retinal degeneration in which the retina loses nearly all of its photoreceptor cells and undergoes major structural changes. Little is known regarding the role the resident glia, the Müller glia, play in the progression of the disease. Here we define gene expression changes in Müller glial cells (MGCs) from two different mouse models of RP, the retinal degeneration 1 (rd1) and rhodopsin knock-out (Rhod-ko) models. The RNA repertoire of 28 single MGCs was comprehensively profiled, and a comparison was made between MGC from wild type (WT) and mutant retinas. Two time points were chosen for analysis, one at the peak of rod photoreceptor death and one during the period of cone photoreceptor death. MGCs have been shown to respond to retinal degeneration by undergoing gliosis, a process marked by the upregulation of GFAP. In this data, many additional transcripts were found to change. These can be placed into functional clusters, such as retinal remodeling, stress response, and immune related response. It is noteworthy that a high degree of heterogeneity among the individual cells was observed, possibly due to their different spatial proximities to dying cells, and/or inherent heterogeneity among MGCs.

2014-10-31 | GSE35386 | GEO

A role for Prenylated rab acceptor 1 in vertebrate photoreceptor development

Project description:The rd1 mouse retina is a well-studied model of retinal degeneration where rod photoreceptors undergo cell death beginning at postnatal day P10 until P21. This period coincides with photoreceptor terminal differentiation in a normal retina. We have used the rd1 retina as a model to investigate early molecular defects in developing rod photoreceptors prior to the onset of degeneration. Using a microarray approach, we performed gene profiling comparing rd1 and wild type retinas at four time points starting at P2, prior to any obvious biochemical or morphological differences, and concluding at P8, prior to the initiation of cell death. We have identified genes that are differentially regulated in the rd1 retina at early time points, which may give insights into developmental defects that precede photoreceptor cell death. This is the first report of PRA1 expression in the retina. Our data support the hypothesis that PRA1 plays an important role in vesicular trafficking between the Golgi and cilia in differentiating and mature rod photoreceptors. Retinal samples were harvested from both rd1/le and wt animals at postnatal days 2, 4, 6, and 8 for microarray. Each sample included 8-14 retinas and experiments were performed in quadruplicate. Ten micrograms of total RNA was used for cDNA systhesis in target molecule production.

2012-11-02 | E-GEOD-41821 | biostudies-arrayexpress

Rod photoreceptors degeneration in the rd1 model of retinitis pigmentosa involves a cascade of events leading to proteasome dysfunction

Project description:Retinitis pigmentosa is an inherited disease with sequential retinal degeneration of rod then cone photoreceptors leading to blindness. As in this human syndrome the rd1 mouse model carries a recessive mutation in the rod-specific cGMP phosphodiesterase beta subunit gene leading to rod followed by cone photoreceptor death. The cascade of early events leading to the induction of rod cell death through apoptosis remains unknown. We report a differential whole-genome expression profiling analysis of the wild-type and rd1 mouse retinal transcriptional program using high-density oligonucleotide microarrays with a time series experiment spanning the entire rod photoreceptor degeneration process. Among the 1252 genes found to be significantly differentially expressed, a key group of 19 loci showed distinct differences in expression early in development, suggesting that these genes of clinical interest may play a fundamental role in the induction of the rod photoreceptor degeneration.

2020-09-25 | GSE62020 | GEO

Single-cell RNA sequencing of the retina in a model of retinitis pigmentosa reveals early responses to degeneration in rods and cones

Project description:In inherited retinal disorders such as retinitis pigmentosa (RP), rod photoreceptor-specific mutations cause primary rod degeneration that is followed by secondary cone death and loss of high-acuity vision. Mechanistic studies of retinal degeneration are challenging because of retinal heterogeneity. Moreover, the detection of early cone responses to rod death is especially difficult due to the paucity of cones in the retina. To resolve heterogeneity in the degenerating retina and investigate events in both types of photoreceptors during primary rod degeneration, we utilized droplet-based single-cell RNA sequencing in an RP mouse model, rd10.

2022-04-13 | GSE183206 | GEO

GENE EXPRESSION CHANGES WITHIN MM-CM-^\LLER GLIAL CELLS DURING RETINITIS PIGMENTOSA

Project description:Retinitis Pigmentosa (RP) is a progressive retinal degeneration in which the retina loses nearly all of its photoreceptor cells and undergoes major structural changes. Little is known regarding the role the resident glia, the MM-CM-<ller glia, play in the progression of the disease. Here we define gene expression changes in MM-CM-<ller glial cells (MGCs) from two different mouse models of RP, the retinal degeneration 1 (rd1) and rhodopsin knock-out (Rhod-ko) models. The RNA repertoire of 28 single MGCs was comprehensively profiled, and a comparison was made between MGC from wild type (WT) and mutant retinas. Two time points were chosen for analysis, one at the peak of rod photoreceptor death and one during the period of cone photoreceptor death. MGCs have been shown to respond to retinal degeneration by undergoing gliosis, a process marked by the upregulation of GFAP. In this data, many additional transcripts were found to change. These can be placed into functional clusters, such as retinal remodeling, stress response, and immune related response. It is noteworthy that a high degree of heterogeneity among the individual cells was observed, possibly due to their different spatial proximities to dying cells, and/or inherent heterogeneity among MGCs. Retinas were dissociated and single Muller Glial Cells were picked under a dissecting microscope using a micropipette based on their distinct morphological shape. Single cell cDNAs were generated and genome wide profiles were obtained by hybridization to Affymetrix 430 2.0 microarrays. Data was normalized using MAS5.0 software. A total of 28 Muller Glial Cells were analyzed and confirmed post hoc by expression of known marker genes.

2014-10-31 | E-GEOD-35386 | biostudies-arrayexpress

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