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Expression data to investigate Costello syndrome using human iPSCs differentiated into astroglial progenitors and astrocytes

ABSTRACT: We used microarrays to compare gene expression between three HRAS-wild type lines (13, 162d, 165d) and three HRAS-G12S mutant lines (7, 8, 16). Arrays were conducted in all lines from iPSC-derived astroglial progenitors at 8 weeks of differentiation, and in wild-type astrocyte lines at 28 weeks of differentiation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE64194 | GEO | 2014/12/16

SECONDARY ACCESSION(S): PRJNA270357

REPOSITORIES: GEO

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Expression data to investigate Costello syndrome using human iPSCs differentiated into astroglial progenitors and astrocytes

Project description:We used microarrays to compare gene expression between three HRAS-wild type lines (13, 162d, 165d) and three HRAS-G12S mutant lines (7, 8, 16). Arrays were conducted in all lines from iPSC-derived astroglial progenitors at 8 weeks of differentiation, and in wild-type astrocyte lines at 28 weeks of differentiation. Cells of the astroglial lineage were generated for RNA extraction and hybridization on Affymetrix Human 1.0 ST microarrays. At each stage, cells were plated as a monolayer and treated with 10ng/ml of CNTF for one week before extraction.

2014-12-16 | E-GEOD-64194 | biostudies-arrayexpress

Proteomic analysis for astroglial exosomes

Project description:LC/MS/MS analysis was performed on astroglial exosome samples (3 biological replicates) to identify proteins expressed on the surface of astroglial exosomes. Thes astroglial exosome samples were purified using size-exclusion column from astrocyte conditioned medium (ACM) of primary astrocyte cultures.

2023-08-10 | PXD040650 | Pride

Sex differences in the developmental patterns of the cortical astroglial cell translatome

Project description:Employing translating ribosome affinity purification with RNA sequencing (TRAPseq) on cortical tissue to isolate astroglial-specific translatome from Aldh1l1-L10-GFP mice and examine sex (male + female) and age (postnatal days 1, 4, 7, 14, 35; adults (9 weeks)) dependent changes in the astroglial translatome.

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Astroglial FMRP deficiency cell-autonomously up-regulates miR-128 and disrupts developmental astroglial mGluR5 signaling (miRNA)

Project description:The loss of fragile X mental retardation protein (FMRP) causes fragile X syndrome (FXS), the most common inherited intellectual disability. How the loss of FMRP alters protein expression and astroglial functions remains essentially unknown. Here we showed that selective loss of astroglial FMRP in vivo up-regulates a brain-enriched miRNA, miR-128-3p, in mouse and human FMRP-deficient astroglia, which suppresses developmental expression of astroglial metabotropic glutamate receptor 5 (mGluR5), a major receptor in mediating developmental astroglia to neuron communication. Selective in vivo inhibition of miR-128-3p in FMRP-deficient astroglia sufficiently rescues decreased mGluR5 function, while astroglial overexpression of miR-128-3p strongly and selectively diminishes developmental astroglial mGluR5 signaling. Subsequent transcriptome and proteome profiling further suggests that FMRP commonly and preferentially regulates protein expression through posttranscriptional, but not transcriptional, mechanisms in astroglia. Overall, our study defines an FMRP-dependent cell-autonomous miR pathway that selectively alters developmental astroglial mGluR5 signaling, unveiling astroglial molecular mechanisms involved in FXS pathogenesis.

2020-09-10 | GSE157724 | GEO

Astroglial FMRP deficiency cell-autonomously up-regulates miR-128 and disrupts developmental astroglial mGluR5 signaling (RNA-Seq)

2020-09-10 | GSE157723 | GEO

Astroglial Hmgb1 regulates postnatal astrocyte morphogenesis and cerebrovascular maturation

Project description:Astrocytes are intimately linked with brain blood vessels, a relationship critical for neuronal function. However, astroglial factors driving these physical and functional associations during postnatal brain development have yet to be identified. By characterizing structural and transcriptional changes in mouse cortical astrocytes during the first two postnatal weeks, we find that high-mobility group box 1 (Hmgb1), normally upregulated with injury and involved in adult cerebrovascular repair, is highly expressed in astrocytes at birth and then decreases rapidly. Astrocyte-selective ablation of Hmgb1 at birth affects astrocyte morphology and endfoot placement, alters distribution of endfoot proteins connexin43 and aquaporin-4, induces transcriptional changes in astrocytes related to cytoskeleton remodeling, and profoundly disrupts endothelial ultrastructure. While lack of astroglial Hmgb1 does not affect the blood-brain barrier or angiogenesis postnatally, it impairs neurovascular coupling and behavior in adult mice. These findings identify astroglial Hmgb1 as a key player in postnatal gliovascular maturation.

2023-07-10 | GSE236429 | GEO

Astroglial Hmgb1 regulates postnatal astrocyte morphogenesis and cerebrovascular maturation

Project description:Astrocytes are intimately linked with brain vessels, a relationship that is critical for neuronal health and function. However, key astroglial molecular factors that drive these physical and functional associations during postnatal brain development have not yet been identified. We characterized structural and transcriptional changes in mouse cortical astrocytes and microvessels during the first two postnatal weeks and found that high-mobility group box 1 (Hmgb1), normally upregulated with injury and involved in adult cerebrovascular repair, was highly expressed in astrocytes at birth to then decreased rapidly. Astrocyte-selective ablation of Hmgb1 in newborn mice affected astrocyte morphology and endfoot placement, induced disruption of endfoot proteins connexin43 and aquaporin-4, induced transcriptional changes in astrocytes, and profoundly altered endothelial cell ultrastructure. While lack of astroglial Hmgb1 did not affect the blood-brain barrier or angiogenesis postnatally, it impaired neurovascular coupling and behavior in adult mice. These findings identify astroglial Hmgb1 as a key player in postnatal gliovascular maturation.

2023-06-13 | GSE224784 | GEO

Inhibition of astroglial NF-kB regulates oligogenesis following spinal cord injury.

Project description:Astrocytes are taking the center stage in neurotrauma and neurological disease as they appear to play a dominant role in the inflammatory processes associated with these conditions. Previously, we reported that inhibiting nuclear factor kappa B (NF-kB) activation in astrocytes, by using a transgenic mouse model (GFAP-IκBα-dn mice), results in improved functional recovery following spinal cord injury (SCI), with increased white matter preservation and axonal sparing. In the present study we sought to determine whether this improvement, due to inhibiting NF-k-B activation in astrocytes, could be the result of enhanced oligogenesis in our GFAP-IκBα-dn mice. To gain insight into the underlying molecular mechanisms, we performed microarray analysis in naïve and 3 days, 3 and 6 weeks following SCI in GFAP-IκBα-dn and wild type (WT) littermate mice. Surprisingly, we found the largest number of genes differentially regulated between GFAP-IκBα-dn and WT mice 6 weeks post-injury. Interestingly, the data suggested that inhibiting astroglial NF-kB alters the inflammatory environment to support oligogenesis. Furthermore, confirmation of microarray data with qPCR and western blotting analysis and using BrdU labeling along with cell specific immunohistochemistry, confocal microscopy and quantitative cell counts, we demonstrate a significant increase in oligogenesis in GFAP-IκBα-dn following SCI. These studies suggest that therapeutic strategies targeting NF-kB activation in the CNS following SCI may promote oligogenesis and remyelination. Wild type (WT) mice - time points naïve, 3 days, 3 weeks, 6 weeks. Transgenic mice (TG) - time points naïve, 3 days, 3 weeks, 6 weeks.

2013-09-01 | E-GEOD-46695 | biostudies-arrayexpress

Astroglial FMRP deficiency cell-autonomously up-regulates miR-128 and disrupts developmental astroglial mGluR5 signaling (miRNA)

Project description:Astroglial FMRP deficiency cell-autonomously up-regulates miR-128 and disrupts developmental astroglial mGluR5 signaling (miRNA)

| PRJNA662569 | ENA

Astroglial Connexin 43 sets the blood brain barrier immune quiescence

Project description:In the brain, a unique homeostatic equilibrium strictly controls immune reactions. In healthy conditions, the immune system poorly communicates with the central nervous system (CNS), immune cell migration across the blood brain barrier (BBB) is kept at a very low level and the unique CNS microenvironment strictly restricts immune reactions. Here, we identified the astroglial gap junction protein Connexin 43 has a new actor of this homeostasis. We showed that genetic inactivation of astroglial Cx43 in the mouse induces expression of a specific set of chemokines and endothelial adhesion molecules leading to neutrophils, macrophages, B and T lymphocytes and mature plasmocytes infiltration at the BBB, and to the development of antigen presentation-related mechanisms, in sterile conditions. Thus, astroglial Cx43 by decreasing the expression of leukocytes adhesion and migration mediators, promotes the immune quiescence of the BBB

2015-03-16 | GSE54458 | GEO

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