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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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			Action	DRS
	SRR6742504.fastq.gz	Fastqsanger.gz
	SRR6742505.fastq.gz	Fastqsanger.gz
	SRR6742506.fastq.gz	Fastqsanger.gz
	SRR6742507.fastq.gz	Fastqsanger.gz
	SRR6742508.fastq.gz	Fastqsanger.gz

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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:Astrocytes are the most abundant glial cells of the central nervous system and have recently been recognized as crucial in the regulation of brain immunity. In most neuropathological conditions, astrocytes are prone to a radical phenotypical change called reactivity, which plays a key role in astrocyte contribution to neuroinflammation. However, how astrocytes regulate brain immunity in healthy conditions is an understudied question. One of the astroglial molecule involved in these regulations might be Connexin 43 (Cx43), a gap junction protein highly enriched in astrocyte perivascular endfeet-terminated processes forming the glia limitans. Indeed, Cx43 deletion in astrocytes (Cx43KO) promotes a continuous immune recruitment and an autoimmune response against an astrocyte protein, without inducing any brain lesion. To investigate the molecular basis of this unique immune response, we characterized the polysomal transcriptome of hippocampal astrocytes deleted for Cx43. Our results demonstrate that, in the absence of Cx43, astrocytes adopt an atypical reactive status with no change in most canonical astrogliosis markers, but with an upregulation of molecules promoting immune recruitment, complement activation as well as anti-inflammatory processes. Intriguingly, while several of these upregulated transcriptional events suggested an activation of the ?-interferon pathway, no increase in this cytokine or activation of related signaling pathways were found in Cx43KO. Finally, deletion of astroglial Cx43 was associated with the upregulation of several angiogenic factors, consistent with an increase in microvascular density in Cx43KO brains. Collectively, these results strongly suggest that Cx43 controls immunoregulatory and angiogenic properties of astrocytes.

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Osteocyte Connexin 43 Hemichannels Influence Bone Marrow Mesenchymal Stromal Cell Fate through Prostagladin E2

Project description:Inhibiting Connexin 43 (Cx43) hemichannels in osteocytes led to a significant increase in adipogenesis and a decrease in osteogenesis in bone marrow mesenchymal stromal cells.

2024-12-16 | GSE252059 | GEO

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

2011-01-06 | GSE23431 | GEO

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

2011-01-06 | E-GEOD-23431 | biostudies-arrayexpress

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.

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

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