ChIP-seq of RNA polymerase II, transcription factors and histone modification in retinal pigment epithelial cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE60024 | GEO | 2014/08/03
SECONDARY ACCESSION(S): PRJNA257297
REPOSITORIES: GEO
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Project description:Retinal pigment epithelial cells are critical for eye function and loss of cell function is linked to age-related blindness. Relatively little is known about the transcriptional regulatory networks in these cells. The datasets presented here are ChIP-seq experiments for RNA polymerase II , transcription factors and histone modifications in human retinal pigment epithelial cells. ChIP-Seq for transcription factors, RNA polymerase, histone modifications and CTCF in retinal pigment epithelial cells
2014-08-03 | E-GEOD-60024 | biostudies-arrayexpress
Project description:T cells that encounter cultured ocular pigment epithelial cells in vitro are inhibited from undergoing T cell receptor-triggered activation. Because retinal pigment epithelial (RPE) cells are able to suppress T-cell activation, we studied whether RPE cells could suppress cytokine production by activated T helper (Th) cells. In this study we showed that primary cultured RPE cells greatly suppressed activation of bystander CD4+ T cells in vitro, especially the cytokine production by the target T helper cells (Th1 cells, Th2 cells, Th17 cells, but not Th3 cells). Cultured RPE cells and RPE-supernatants significantly suppressed IL-17 producing CD4+ T cells, and RPE cells fully suppressed polarized Th17 cell lines that induced by recombinant proteins, IL-6 and TGFb2. Moreover, RPE cells failed to suppress IL-17 producing T cells in the presence of rIL-6. In addition, Th17 cells exposed to RPE were suppressed via TGFb, which produce RPE cells. These results indicate that retinal PE cells have immunosuppressive capacity in order to inhibit Th17-type effector T cells. Thus, ocular resident cells play a role in establishing immune regulation in the eye. Retinal pigment epithelium suppresses Th17 cells
2012-07-11 | E-GEOD-22877 | biostudies-arrayexpress
Project description:Retinitis Pigmentosa is a group of inherited eye disorders characterized by progressive degeneration of photoreceptor cells in the retina, leading to vision loss and eventual blindness. One of the known genetic mutations associated with RP is the c.6926A>C mutation in the RPE (retinal pigment epithelium) cells. The dataset involves multiple experimental approaches and cell types, providing a comprehensive understanding of the disease and potential corrective strategies.
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Project description:The retinal pigment epithelium (RPE) is a monolayer of polarized epithelial cells lying between the retina and the choroid/sclera, with a major function in supporting photoreceptor homeostasis, but the role of RPE in eye size regulation is yet to be further explored. it was recently reported that selective deletion of Low density lipoprotein receptor-related protein 2 (Lrp2) in the mouse RPE resulted in large eyes, similar to the phenotypes of Lrp2 whole eye knockout mice, suggesting that the RPE is the tissue in which LRP2 functions. Here, to investigate which downstream pathways of Srebp2 and Lrp2 are responsible for regulating eye growth, we performed RNA-seq analysis with the mouse RPE tissues. Postnatal day 0 (P0) mice were injected with AAV8-Best1-GFP/nSrebp2/ctrl sh/Lrp2 sh1/Lrp2 sh2 viruses to overexpress the constitutively active form of Srebp2 or to knockdown Lrp2 in the RPE specifically. At P14, RPE cells were carefully dissociated for RNA extraction. Via RNA-seq analysis and functional validation, we identified that Bmp2 is the target and the effector of the Srebp2-Lrp2 pathway. Overall, the present study unveils an essential role of RPE in regulating eye size via the Srebp2-Lrp2-Bmp2 signaling pathway, shedding light on the underlying mechanism of eye size control.
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Project description:MicroRNA expression in the mouse eye.MicroRNAs (miRNAs) are key regulators of biological processes. To define miRNA function in the eye, it is essential to determine a high-resolution profile of their spatial and temporal distribution. In this report, we present the first comprehensive survey of miRNA expression in ocular tissues, using both microarray and RNA in situ hybridization (ISH) procedures. We initially determined the expression profiles of miRNAs in the retina, lens, cornea and retinal pigment epithelium of the adult mouse eye by microarray. Each tissue exhibited notably distinct miRNA enrichment patterns and cluster analysis identified groups of miRNAs that showed predominant expression in specific ocular tissues or combinations of them. Next, we performed RNA ISH for over 220 miRNAs, including those showing the highest expression levels by microarray, and generated a high-resolution expression atlas of miRNAs in the developing and adult wild-type mouse eye, which is accessible in the form of a publicly available web database. We found that 122 miRNAs displayed restricted expression domains in the eye at different developmental stages, with the majority of them expressed in one or more cell layers of the neural retina . This analysis revealed miRNAs with differential expression in ocular tissues and provided a detailed atlas of their tissue-specific distribution during development of the murine eye. The combination of the two approaches offers a valuable resource to decipher the contributions of specific miRNAs and miRNA clusters to the development of distinct ocular structures. microRNA profiling of ocular tissues from mouse. In particular we analysed the cornea, lens, Retina Pigment Epithelium (RPE) and retina and compared them against RNA extracted from the entire eye. The purpose of this experiment was to understand which microRNAs are present nd/or show differential expression in the various structures of the eye (cornea, lens, RPE, retina). The samples numbered 1 & 2 (i.e. CORNEA1, CORNEA2 etc ) are biological replicates, prepared from tissues dissecyed from different groups of wild-type animals. RNA extracted from the entire eye (EYE) served as the unique reference sample. For each tissue to be analysed we performed the following hybridizations: - 2 slides for lens (LENS1, LENS2) vs entire eye (EYE) - 2 slides for RPE (RPE1, RPE2) vs entire eye (EYE) - 2 slides for retina (RETINA1, RETINA2) vs entire eye (EYE) - 2 slides for cornea (CORNEA1, CORNEA2) vs entire eye (EYE) - 1 slide for entire eye (EYE) vs entire eye (EYE)
2010-11-22 | E-GEOD-22882 | biostudies-arrayexpress
Project description:We generated a retinal pigment epithelial cell line with complete knockout of giantin using CRISPR. This experiment sought to define changes in the transcriptome of that cell line compared to the parental wild-type cells.
2017-10-01 | E-MTAB-5618 | biostudies-arrayexpress
Project description:Oxidative stress has been implicated in the pathogenesis of age-related macular degeneration(AMD), the leading cause of blindness in the elderly, with retinal pigment epithelial (RPE) cells playing a key role. To better understand the cytotoxic mechanisms underlying oxidative stress, we used cell culture and mouse models of iron overload, as iron can catalyze reactive oxygen species formation in the RPE. Iron-loading of cultured iPS-RPE cells increased lysosomal abundance, impaired proteolysis, and reduced the activity of a subset of lysosomal enzymes,including lysosomal acid lipase and acid sphingomyelinase. In a murine model of systemiciron overload, RPE cells accumulated lipid peroxidation adducts and lysosomes, developed progressive hypertrophy, and underwent cell death. Proteomic and lipidomic analyses revealed accumulation of lysosomal proteins, ceramide biosynthetic enzymes, and ceramides. The proteolytic enzyme cathepsin D had impaired maturation. A large proportion oflysosomes were galectin-3 positive, suggesting cytotoxic lysosomal membrane permeabilization (LMP). Collectively, these results demonstrate that iron overload induces lysosomal accumulation and impairs lysosomal function, likely due to iron-induced lipid peroxides that can inhibit lysosomal enzymes.
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Project description:The integrity of the epithelium is maintained by a complex but regulated interplay of processes that allow seamless orchestration of a proliferative state into a stably differentiated state. In this study, using stem cell derived Retinal Pigment Epithelium (RPE) cells as a model; we have investigated the molecular mechanisms that affect attainment of the epithelial phenotype. We identify a novel role for the proto-oncogene FOXM1 in determining epithelial fate of RPE by directly regulating cell proliferation and by indirectly regulating expression of signalling factors BMP7 and Wnt5B; both of which are intimately required for eventual acquisition of the epithelial phenotype. This study uncovers the role of FOXM1 in a non-oncogenic, native-like setting and shows that human ES derived RPE can serve as a useful model system to address biological questions not restricted to visual function.
2015-07-24 | E-MTAB-3137 | biostudies-arrayexpress
Project description:T cells that encounter cultured ocular pigment epithelial cells in vitro are inhibited from undergoing T cell receptor-triggered activation. Because retinal pigment epithelial (RPE) cells are able to suppress T-cell activation, we studied whether RPE cells could suppress cytokine production by activated T helper (Th) cells. In this study we showed that primary cultured RPE cells greatly suppressed activation of bystander CD4+ T cells in vitro, especially the cytokine production by the target T helper cells (Th1 cells, Th2 cells, Th17 cells, but not Th3 cells). Cultured RPE cells and RPE-supernatants significantly suppressed IL-17 producing CD4+ T cells, and RPE cells fully suppressed polarized Th17 cell lines that induced by recombinant proteins, IL-6 and TGFb2. Moreover, RPE cells failed to suppress IL-17 producing T cells in the presence of rIL-6. In addition, Th17 cells exposed to RPE were suppressed via TGFb, which produce RPE cells. These results indicate that retinal PE cells have immunosuppressive capacity in order to inhibit Th17-type effector T cells. Thus, ocular resident cells play a role in establishing immune regulation in the eye.
2012-07-12 | GSE22877 | GEO
Project description:RNAseq of human retinal pigment epithelial cells/choroid
| PRJNA752566 | ENA