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Gene expression changes under cyclic mechanical stretch in rat retinal Muller cells

ABSTRACT: The retina is often subjected to tractional forces in a variety of conditions, for instance, pathological myopia, proliferative vitreoretinopathy. As the predominant glial element in the sensory retina, Muller cells are responsible for the homeostatic and metabolic support of retinal neurons and active players in virtually all forms of retinal injury and disease. Besides, Muller cells span the entire retinal thickness, extending from the inner to the outer limiting membranes, with cell bodies located in the inner nuclear layer and lateral processes expanding into the plexiform layers of the tissue. Because of this unique morphology, Muller cells can sense even minute changes in the retinal structure because of the mechanical stretching of their long processes or side branches. Thus, it’s reasonable to infer that Muller cells also participate in ocular diseases when the retina is overstretched. In this study, we aim to investigate the whole genome regulation of Muller cells under mechanical stretching, which may help in excluding possible molecular mechanisms that would account for many retinal diseases in which the retina is often subjected to mechanical forces. We used microarrays to identify patterns of gene expression changes induced by cyclic mechanical stretching in Muller cells.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE43516 | GEO | 2013/01/16

SECONDARY ACCESSION(S): PRJNA186631

REPOSITORIES: GEO

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Gene expression changes under cyclic mechanical stretch in rat retinal Muller cells

Project description:The retina is often subjected to tractional forces in a variety of conditions, for instance, pathological myopia, proliferative vitreoretinopathy. As the predominant glial element in the sensory retina, Muller cells are responsible for the homeostatic and metabolic support of retinal neurons and active players in virtually all forms of retinal injury and disease. Besides, Muller cells span the entire retinal thickness, extending from the inner to the outer limiting membranes, with cell bodies located in the inner nuclear layer and lateral processes expanding into the plexiform layers of the tissue. Because of this unique morphology, Muller cells can sense even minute changes in the retinal structure because of the mechanical stretching of their long processes or side branches. Thus, itM-bM-^@M-^Ys reasonable to infer that Muller cells also participate in ocular diseases when the retina is overstretched. In this study, we aim to investigate the whole genome regulation of Muller cells under mechanical stretching, which may help in excluding possible molecular mechanisms that would account for many retinal diseases in which the retina is often subjected to mechanical forces. We used microarrays to identify patterns of gene expression changes induced by cyclic mechanical stretching in Muller cells. Rat Muller cells were seeded onto flexible bottom culture plates and subjected to a cyclic stretching regimen of 15% equibiaxial stretching for 1 and 24 h.Muller cells cultured under the same conditions but with no applied mechanical strain were considered as the unstretched control. At each time points (1 and 24 h), three totally independent experiments (3 stretched samples and 3 control samples) were conducted. Muller cells were selected for RNA extraction and hybridization on Affymetrix microarrays. Stretch (S); Control (C)

2013-01-16 | E-GEOD-43516 | biostudies-arrayexpress

Hypoxia tolerance in the Norrin-deficient retina and the chronically hypoxic brain stuied at single-cell resolution

Project description:The mammalian central nervous system (CNS) is capable of tolerating chronic hypoxia, but cell type-specific responses to this stress have not been systematically characterized. In the Norrin-knockout (NdpKO) mouse, a model of familial exudative vitreoretinopathy (FEVR), developmental hypovascularization of the retina produces chronic hypoxia of inner nuclear layer (INL) neurons and Muller glia. We have used single-cell RNA sequencing, untargeted metabolomics, and metabolite labeling from 13C-glucose to compare wild type and NdpKO retinas. In NdpKO retinas, we observe gene expression responses consistent with hypoxia in Muller glia and retinal neurons, and we find a metabolic shift that combines reduced flux through the tricarboxylic acid cycle with increased synthesis of serine, glycine, and glutathione. We also used single-cell RNA sequencing to compare the responses of individual cell types in NdpKO retinas to those in the hypoxic cerebral cortex of mice that were housed for one week in a reduced oxygen environment (7.5% oxygen). In the hypoxic cerebral cortex, glial transcriptome responses most closely resemble the response of Muller glia in the NdpKO retina. In both retina and brain, vascular endothelial cells activate a previously dormant tip cell gene expression program, which likely underlies the adaptive neo-angiogenic response to chronic hypoxia. These analyses of retina and brain transcriptomes at single-cell resolution reveal both shared and cell-type-specific changes in gene expression in response to chronic hypoxia, implying both shared and distinct cell type-specific physiologic responses.

2019-04-19 | GSE125708 | GEO

Expression data from adult mouse normal and damaged retina from B6 and 129 mouse strains

Project description:Retinal damage causes proliferation of Muller glia, but the degree of proliferation depends on mouse strains. Muller glial proliferation was significantly promoted by the addition of GSK3 inhibitor in 129, but not in B6. We used retinal explant culture as a model for retinal damage which caused preferential photoreceptor death in a few days. We used microarrays to detail the global programme of gene expression regulating the proliferative potential of Muller glia after retinal damage. Total RNA from intact whole retina, retinal tissue cultured for three days, and retinal tissue cultured with chir99021 for three days was used. Retinal tissues from 10 weeks old mice were used.

2014-03-06 | E-GEOD-54056 | biostudies-arrayexpress

Single cell transcriptomic comparison of human fetal retina, hPSC-derived retinal organoids, and long-term retinal cultures.

Project description:To study the development of human retina, we used single cell RNAseq at key fetal stages and followed the development of the major cell types, as well as populations of transitional cells. We also analyzed stem cell (hPSC)-derived retinal organoids; although organoids have a very similar cellular composition at equivalent ages to the fetal retina, there are some differences in gene expression of particular cell types. Moreover, the inner retinal lamination is disrupted in more advanced stages of organoids when compared with fetal retina. To determine whether the disorganization in the inner retina was due to the culture conditions, we analyzed retinal development in fetal retina maintained under similar conditions. These retinospheres develop for at least 6 months, displaying better inner retinal lamination than retinal organoids. Our scRNAseq comparisons between fetal retina, retinal organoids and retinospheres provide a new resource for developing better in vitro models for retinal disease.

2020-01-10 | GSE142526 | GEO

Mechanisms of stretch-mediated skin expansion at single cell resolution [ATAC-seq]

Project description:The ability of the skin to expand in response to stretching has, for decades, been exploited in reconstructive surgery. Several studies have investigated the response of stretching epidermal cells in vitro. However, it remains unclear how mechanical forces affect epidermal stem cell behaviour in vivo. Here, we develop a mouse model in which the temporal consequences of the stretching the skin epidermis can be studied. Using a multidisciplinary approach that combines clonal analysis and mathematical modelling, we show that mechanical force induces skin expansion by promoting the renewal of epidermal stem cells. This occurs through a structured response in which cell fates are coordinated locally by stem cells that switch between states primed for renewal or differentiation. Transcriptional and chromatin profiling identifies the gene regulatory networks modulated by mechanical force. Using a combination of pharmacological inhibition and several conditional gene loss-of-function mouse mutants, we dissect the signalling pathways that control force-mediated tissue expansion.

2020-05-18 | GSE126734 | GEO

The alarmin IL-33 amplifies an immune response in the degenerating retina

Project description:ST2 heterodimerizes with IL-1RAcp to form the receptor for IL-33, which is primarily associated with allergic inflammation by inducing Th2 responses. Recently, however, IL-33 was found to be expressed in the central nervous system and in retinal Muller cells which imply functions, as yet undescribed, beyond Th2 mediated inflammation. Muller cells support the health of the retina and photoreceptors and are also involved in inflammation in retinal degeneration. It is not known how IL-33/ST2 functions in this capacity. We recently found that ST2 ko mice are protected from CLE-induced photoreceptor loss, implying a detrimental effect of IL33/ST2 in CLE. We wish to perform microarray analysis using WT and ST2 KO mice in CLE model to better understand the mechanism by which IL-33/ST2 regulates retinal degeneration. CLE (Constant Light Exposure) is a model of retinal damage/degeneration in mice. Mice are exposed to bright light 24 hours a day for a period of time which damages retina photoreceptors. This damage is assessed by histology, optical coherence tomography (OCT), which measures retina thickness in vivo. In this experiment, the WT and ST2 KO mice (5 mice per genotype per time point) will be exposed to 1200-lux constant light for 0, 3, 10 days. The retinal RNA will be isolated and analyzed for differential gene expression by microarray.

2015-12-17 | E-GEOD-74695 | biostudies-arrayexpress

Transcriptome analysis of the uninjured Muller glia (MG) and MG derived retinal progenitors at 4 day post injured zebrafish retina

Project description:The study was aimed at comparing the transcriptome of MG cells of the retina with the progenitors derived from them after an injury. This information will help in the identification of factors that are responsible for the retinal regeneration. Muller glia were isolated by fluorescent activated cell sorting (FACS) using uninjured retinas from transgenice zebrafish (gfap:gfp) where green florescent protein (GFP) is under the control of the glial fibrillary acidic protein (gfap) promoter. MG-derived retinal progenitors were isolated by FACS at 4 days post retinal injury from 1016 tuba1a:gfp transgenic fish where GFP is driven by the tuba1a promoter which is specifically activated in these progenitors. Total RNA was isolated from these cell populations and subjected to microarray analysis to compare their transcriptomes. Samples were prepared in duplicate.

2012-08-09 | E-GEOD-36191 | biostudies-arrayexpress

Single Cell RNA-sequencing of murine back skin interfollicular epidermis basal cells

Project description:The ability of the skin to grow in response to stretching has, for decades, been exploited in reconstructive surgery. The response of epidermal cells to stretching has been studied in vitro. However, it remains unclear how mechanical forces affect epidermal cell behaviour in vivo. Here, we develop a mouse model in which the consequences of stretching on skin epidermis can be studied. Using a multidisciplinary approach that combines clonal analysis with quantitative modelling and single-cell RNA-seq, we show that stretching induces skin expansion by a transient bias in the renewal activity of epidermal stem cells, while a second subpopulation of basal progenitors remains committed to differentiation. Transcriptional and chromatin profiling identifies how cell states and gene regulatory networks are modulated by stretching. Using pharmacological inhibitors and mouse mutants, we define the mechanisms that control stretch-mediated tissue expansion.

2020-05-18 | GSE146637 | GEO

Phosphoproteome of cyclic stretch A549 and IMR-90

Project description:Lung cancer is one of the leading causes of death. However, most of the researches were based on the traditional cell-culturing method. Whereas cells of lung are subjected to the mechanical forces periodically while breathing. In the present study, we applied cyclic stretch to stimulate the continuously contracting physical condition. We uncovered the stretching force-induced phosphoproteome in lung cancer cell A549 and fibroblast IMR-90. 2048 and 2604 phosphosites corresponding to 837 and 1008 phosphoproteins were identified in A549 and IMR-90, respectively. Interestingly, cytoskeleton reorganization and mitochondrial localization were enriched in the significantly expressed phosphoproteins in response to cyclic stretch. Indeed, we found this physical stress changed cell alignment thus disrupted mitochondrial dynamics. We proved that mitochondrial fusion is induced by uniaxial stretch in 2 cell lines. This study reveals the molecular mechanism of cyclic stretch and supports that stretching force enhanced cellular rearrangement and mitochondrial fusion in lung cells.

2021-09-08 | PXD012010 | Pride

Mechanisms of stretch-mediated skin expansion at single cell resolution [array]

2020-05-18 | GSE126231 | GEO

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