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Paracrine effects of estrogen on 231BR cells, through ER+ astrocytes

ABSTRACT: The objective of this study was to determine the extent to which paracrine action of 17-beta-estradiol on ER+ mouse astrocytes, affect gene expression of MDA231-derived brain trophic 231BR cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE71272 | GEO | 2016/07/31

SECONDARY ACCESSION(S): PRJNA290777

REPOSITORIES: GEO

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Paracrine effects of estrogen on 231BR cells, through ER+ astrocytes

Project description:The objective of this study was to determine the extent to which paracrine action of 17-beta-estradiol on ER+ mouse astrocytes, affect gene expression of MDA231-derived brain trophic 231BR cells. Microarray analysis was performed in triplicate samples from 231BR cells treated with vehicle (OH), 10nM Estradiol (E2), alone or in combination with mouse astrocytes. 231BR-EGFP cells were sorted after 24h co-culture.

2016-07-31 | E-GEOD-71272 | biostudies-arrayexpress

Homo sapiens

Project description:Paracrine effects of estrogen on 231BR cells, through ER+ astrocytes

| PRJNA290777 | ENA

Activity-dependent cholesterol biosynthesis in human-derived astrocytes regulates the functional maturation of human-derived cortical neurons

Project description:Astrocytes regulate the functional maturation of neurons by providing trophic support, regulating membrane properties and coordinating synapse formation. However, it is unclear to what degree astrocytes use activity-dependent mechanisms in these intercellular signalling processes. Using an induced pluripotent stem cell system and long-term optogenetic stimulation of human astrocytes, we reveal that activity-dependent astrocytic signals enhance the functional maturation of human cortical neurons, through increases in synaptic connectivity and excitability. Transcriptomic analyses determine that this involves the activity-dependent up-regulation of cholesterol synthesis – a process ascribed to astrocytes, which regulates neuronal maturation. Up-regulated astrocyte genes encode enzymes and transcription factors that control the levels of cholesterol synthesis. Biochemical assays confirm an activity-dependent upregulation of cholesterol synthesis in astrocytes, which is required for the maturational effects upon neurons. Thus, we reveal a novel mechanism that may dynamically match astrocyte function to neuronal needs, and identify targets for modulating cholesterol synthesis in the CNS.

2023-07-21 | GSE236398 | GEO

RNA-seq of iPSC-derived astrocytes that are capable of exerting pro-maturational effect on synaptic networks

Project description:Astrocytes interact closely with neurons and facilitate neuronal maturation and function by providing trophic support, regulating the extracellular environment, and engaging in a variety of inter-cellular signalling mechanisms. We have described the generation of human astrocytes and neurons from a common cortical progenitor pool, thereby recapitulating aspects of in vivo development. Firstly, we show that the iPSC-derived astrocytes exhibit many of the key molecular and functional hallmarks predicted of astrocytes. Secondly, we provide functional and transcriptomic analyses of the astrocytes’ capacity to interact with neurons both through rapid regulation of ongoing synaptic transmission as well as exerting pro-maturational effects on the synaptic networks. Transcriptional analysis included the comparison of the present RNA-seq of iPSC-derived astrocytes to other iPSC-derived astrocyte datasets as well as fetal and adult human astrocytes. We investigated differences in gene expression between our maturation-enhancing iPSC-astrocytes and iPSC-astrocytes previously shown to be unable to promote synaptic network maturation. By integrating transcriptomic data, functional genomic annotations and protein-protein interaction resources we support that astrocytic extracellular signalling is important for the ability of astrocytes to mediate functional neuronal maturation. This work provides a foundation for future investigations into astrocyte-neuron interactions in human health and disease.

2020-04-30 | GSE149598 | GEO

Expression data from paracrine senescence

Project description:Senescence can be transmitted in a paracrine way from cells undergoing Oncogene Induced Senescence (OIS) to naM-CM-/ve normal cells. We define this phenomenon as M-bM-^@M-^\paracrine senescenceM-bM-^@M-^] We used microarrays to compare the trancriptome of cells undergoing paracrine senescence to the transcriptome of cells suffering OIS to unveil the common signatures defining both events and the similarities between them IMR90 cells were co-cultured with IMR90 ER:RAS undergoing OIS or IMR90-Vector control cells using 0.2 M-NM-<m pore transwell (anopore) to allow communication of soluble factors but physical separation of the two cell populations. The total mRNA of IMR90, IMR90 ER:RAS or IMR90 cells cultured in Transwells together with IMR90 vector or IMR90 ER:RAS cells during 7 days in the presence of 200 nM 4OHT and 0.5 % FBS was extracted and hybridized on Affymetrix microarrays to compare paracrine senescence to OIS.

2013-06-13 | E-GEOD-41318 | biostudies-arrayexpress

Expression data from paracrine senescence

Project description:Senescence can be transmitted in a paracrine way from cells undergoing Oncogene Induced Senescence (OIS) to naïve normal cells. We define this phenomenon as “paracrine senescence” We used microarrays to compare the trancriptome of cells undergoing paracrine senescence to the transcriptome of cells suffering OIS to unveil the common signatures defining both events and the similarities between them

2013-06-13 | GSE41318 | GEO

Astrocytes

Project description:Astrocytes Raw sequence reads

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Transcriptome alterations induced by steroid receptors agonists in primary neurons and astrocytes

Project description:We utilized whole-genome microarrays (Illumina Mouse WG-6) to measure changes in mRNA abundance levels induced by steroid hormones in primary neurons and astrocytes. To stimulate gene expression we treated neuronal and astroglial cultures with glucocorticoid receptor agonist (dexamethasone), mineralocorticoid (aldosterone), progesterone (progesterone), androgen (5α-dihydrotestosterone) and estrogen 2 (β-estradiol). Keywords: Hormonal response

2016-05-01 | GSE78281 | GEO

RNA-Seq of wild-type murine primary cortical neurons co-cultured in a transwell-based system with Mecp2 knock-out or wild-type cortical murine astrocytes

Project description:Rett syndrome (RTT; OMIM#312750) is a rare devastating neurodevelopmental disorder that represents the most common genetic cause of severe intellectual disability in girls. Mutations in the X-linked methyl-CpG-binding protein 2 (MECP2) gene have been reported in over 95% cases of classical forms of RTT. Although initial studies supported a role for MeCP2 exclusively in neurons, recent data indicate a function also in astrocytes, which emerged as critical players involved in RTT pathogenesis through non-cell autonomous effects. Indeed, Mecp2 knock-out (KO) astrocytes cannot properly support neuronal maturation of wilt-type (WT) neurons and our data demonstrated a detrimental effect also on synaptogenesis and synaptic maintainence. Nevertheless, the molecular mechanisms by which RTT astrocytes can impact on neuronal health remains unknown. In comparison to previous studies exploring the transcriptomic and proteomic profiles of KO astrocytes per se, we used an indirect strategy to unveil the molecular mechanisms responsible for their negative action on neurons. We thus analysed the molecular pathways deregulated in WT neurons cultivated under the influence of KO (n=8) versus WT (n=7) astrocytes, in a transwell-based co-culture system, that allows the exchange of paracrine signals preventing cell-to-cell contact. Astrocytes were seeded on transwell inserts and transferred on neurons at Div0; the co-cultures were maintained until Div14. WT cortical neurons cultivated alone were also included (n=5).

2024-02-19 | E-MTAB-12393 | biostudies-arrayexpress

Analysis of estrogen-induced mRNA in endometrial cancer cells with forced expression of ER

Project description:We used the endometrial adenocarcinoma cell line in which the ERα cDNA gene was transfected and forcedly expressed ER. Then the factors induced by estrogen (Estradiol: E2) were measured by microarray.

2022-03-08 | GSE197905 | GEO

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