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Connexin 43 controls the immunoregulatory phenotype of astrocytes

ABSTRACT: Connexin 43 controls the immunoregulatory phenotype of astrocytes

PROVIDER: PRJNA434418 | ENA |

REPOSITORIES: ENA

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Connexin 43 controls the immunoregulatory phenotype of astrocytes

Project description:BAC array purification of hippocampus astroglial ribosome-bound transcriptome in astrocytes from Aldh1l1:Rpl10a eGFP/ Cx43 KO and Aldh1l1:Rpl10a eGFP/ Cx43FL mice

2019-05-22 | GSE110721 | GEO

Connexin 43 Controls the Astrocyte Immunoregulatory Phenotype.

Project description: Not available

| S-EPMC5924386 | biostudies-literature

Co-IP (AP-MS) of Connexin-43 - Gap junction protein Connexin-43 is a direct transcriptional regulator of N-cadherin in vivo

Project description:Co-IP Experiment Bait: Cx43-Flag Cell line: Hela Related Publication: Gap Junction protein Connexin-43 is a direct transcriptional regulator of N-cadherin in vivo, Maria Kotini, Elias Barriga, Jonathan Leslie, Marc Gentzel, Verena Rauschenberger, Alexandra Schambony, and Roberto Mayor

2018-10-16 | PXD010870 | Pride

Connexin 43-mediated neurovascular interactions regulate neurogenesis in the adult brain subventricular zone.

Project description:To gain a deeper understanding of the Connexin (Cx)-43-dependent molecular regulation of neural stem behavior, we used scRNAseq approach on endothelial cells (ECs) and neural stem and progenitor cells (NSPCs) from knock out mice.

2023-03-02 | GSE221558 | GEO

Sertoli cell specific testicular gene expression of Connexin 43 knockout mice

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Mutant TDP-43 in Astrocytes Kills Motor Neurons in Rats through Neurotoxic Gain and Neuroprotective Loss in Astrocytes

Project description:Mutation in TDP-43 is causative to amyotrophic lateral sclerosis (ALS). TDP-43 is a multifunctional ribonucleoprotein and is reproted to regulate thousands of genes in neurons, but how astrocytes contribute to TDP-43 pathogenesis is not known. This study examined how mutant TDP-43 in astrocytes kills motor neurons and causes ALS phenotypes. Primary astrocytes were isolated from transgenic rats expressing mutant TDP-43 or from control rats without mutant TDP-43 expression. Cultured astrocytes were induced to express mutant human TDP-43 and their gene expression profiles were determined by microarray assays. Microarray analysis revealed that hundreds of genes were altered in astrocytes in response to mutant TDP-43 expression. As mutant TDP-43 transgene is under the control of tetracycline-regulated pomoter elements (TRE), mutant TDP-43 expression is subjected to Doxycline regulation. Astrocytes isolated from GFAP-tTA/TRE-TDP43M337V rats were desiginated as M337V groups and astrocytes isolated from GFAP-tTA single transgenic rats were desiginated as tTA control groups. Total RNA was isolated from cultured astrocytes at varying times (3, 4, or 6 days after Dox withdrawal) after mutant TDP-43 was induced in astrocytes. Upon mutant TDP-43 induction in astroyctes, gene expression profiles in astroyctes were determined by Illumina Direct Hybridization Assay and compared between tTA and M337V groups at the varying time points of mutant TDP-43 induction.

2013-05-20 | E-GEOD-42091 | biostudies-arrayexpress

Sertoli cell specific testicular gene expression of Connexin 43 knockout mice

Project description:Infertility observed in adult Sertoli cell (SC)-specific Connexin 43 Knockout-mice rather seems to be an effect of the disturbed SC-Germ cell (GC) crosstalk than a direct consequence of the loss of Cx43 protein in SC with important GC specific genes being mostly affected by this deletion. Identification of differentially expressed genes in testis of cx43 KO-mice at developmental stage 8 days post partum when compared with testis of WT-mice

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Loss of TDP-43 in astrocytes leads to motor deficits by triggering A1-like reactive phenotype and tri-glial dysfunctions

Project description:The majority of patients with amyotrophic lateral sclerosis (ALS) have abnormal TDP-43 aggregates in the nucleus and/or cytosol of their surviving neurons and glia. Although accumulating evidence indicates that astroglial dysfunctions contribute to motor neuron degeneration in ALS, the normal physiological functions of TDP-43 in astrocytes are largely unknown and whether the loss of astroglial TDP-43 contributes to ALS remains to be clarified. Here, we showed that TDP-43 deleted astrocytes showed cell-autonomously enhanced GFAP immunoreactivity without affecting astrocyte or microglia proliferation. At the transcriptomic level, TDP-43 deleted astrocytes resemble the A1-reactive astrocytes and induce microglia to increase C1q expression. These astrocytic changes do not cause the loss of motor neurons in spinal cords or denervation at the neuromuscular junctions. In contrast, there was a selective reduction of mature oligodendrocytes, but not oligodendrocyte precursor cells, suggesting a tri-glial dysfunction mediated by TDP-43-deleted astrocytes. Mice with astroglial TDP-43 deletion developed motor, but not sensory, deficits. Taken together, our results demonstrate that TDP-43 is required to maintain the protective functions of astrocytes relevant to the development of motor deficits in mice.

2020-11-01 | GSE156542 | GEO

Mutant TDP-43 in Astrocytes Kills Motor Neurons in Rats through Neurotoxic Gain and Neuroprotective Loss in Astrocytes

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Project description:TDP-43 is an RNA binding protein involved in amyotrophic lateral sclerosis and other neurodegenerative diseases. The purpose of this study was to determine if loss of TDP-43 function leads to accumulation of repetitive element transcripts, double-stranded RNA (dsRNA) and innate immune activation that may be involved in disease pathology. TDP-43 was knocked down in primary rat astrocytes via siRNA, cells were treated with/without ATP (an immune modulator), and polyA RNA-seq was performed to profile gene expression. Immunoprecipitation/RNA-seq was also performed using a dsRNA-specific antibody to identify potential dsRNAs resulting from TDP-43 knockdown.

2019-08-09 | GSE135611 | GEO

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