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Connexin 30 deficiency attenuates A2 astrocyte responses and induces severe neurodegeneration in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride Parkinson’s disease animal model

ABSTRACT: Connexin 30 deficiency attenuates A2 astrocyte responses and induces severe neurodegeneration in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride Parkinson’s disease animal model

PROVIDER: PRJNA453681 | ENA |

REPOSITORIES: ENA

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Connexin 30 deficiency attenuates A2 astrocyte responses and induces severe neurodegeneration in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride Parkinson’s disease animal model

Project description:Cx30 deficiency induced acceleration of dopaminergic neuron death upon MPTP toxicity. Gene expressions in the striatum of wild type and Cx30 KO mice after MPTP treatment were different in the aspect of neuroprotective A2 response.

2018-06-01 | GSE113693 | GEO

Connexin 30 deficiency attenuates A2 astrocyte responses and induces severe neurodegeneration in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride Parkinson's disease animal model.

Project description: Not available

| S-EPMC6090688 | biostudies-literature

Dysregulation of Gene Expression in the 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Lesioined Mouse Substantia Nigra

Project description:Parkinson's disease pathogenesis proceeds through several phases, culminating in the loss of dopaminergic neurons of the substantia nigra (SN). Although the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of oxidative SN injury is frequently used to study degeneration of dopaminergic neurons in mice and non-human primates, an understanding of the temporal sequence of molecular events from inhibition of mitochondrial complex 1 to neuronal cell death is limited. Here, microarray analysis and integrative data mining were used to uncover pathways implicated in the progression of changes in dopaminergic neurons after MPTP administration. This approach enabled the identification of small, yet consistently significant, changes in gene expression within the SN of MPTP-treated animals. Such an analysis disclosed dysregulation of genes in three main areas related to neuronal function: cytoskeletal stability and maintenance, synaptic integrity, and cell cycle and apoptosis. The discovery and validation of these alterations provide molecular evidence for an evolving cascade of injury, dysfunction, and cell death. Keywords: Parkinson's disease; MPTP; gene expression; microarray; cytoskeleton; mouse

2006-05-12 | GSE4788 | GEO

Transcription profiling of mouse with ablation of connexin 30 in the stria vascularis

Project description:Effect of the ablation of connexin 30 in the stria vascularis

2007-04-16 | E-MEXP-558 | biostudies-arrayexpress

Neurodegeneration and Neuroinflammation are Linked, but Independent of α-Synuclein Inclusions, in a Seeding/Spreading Mouse Model of Parkinson’s Disease

Project description:A key process of neurodegeneration in Parkinson's disease (PD) is the transneuronal spreading of alpha-synuclein. Alpha-synuclein is a presynaptic protein that is implicated in the pathogenesis of PD and other synucleinopathies, where it forms, upon intracellular aggregation, pathological inclusions. Other hallmarks of PD include neurodegeneration and microgliosis in susceptible brain regions. Whether it is primarily transneuronal spreading of a-synuclein particles, inclusion formation, or other mechanisms, such as inflammation, that cause neurodegeneration in PD is unclear. We used spreading/aggregation of alpha-synuclein induced by intracerebral injection of a-synuclein preformed fibrils into the mouse brain to address this question. We performed quantitative histological analysis for a-synuclein inclusions, neurodegeneration, and microgliosis in different brain regions, and a gene expression profiling of the ventral midbrain, at two different timepoints after disease induction. We observed significant neurodegeneration and microgliosis in brain regions not only with, but also withouta-synuclein inclusions. We also observed prominent microgliosis in injured brain regions that did not correlate with neurodegeneration nor with inclusion load. In longitudinal gene expression profiling experiments, we observed early and unique alterations linked to microglial mediated inflammation that preceded neurodegeneration, indicating an active role of microglia in inducing neurodegeneration. Our observations indicate that a-synuclein inclusion formation is not the major driver in the early phases of PD-like neurodegeneration, but that diffusible, oligomeric a-synuclein species, which induce unusual microglial reactivity, play a key role in this process.

2020-11-02 | GSE155716 | GEO

Mapping the anti-cancer activity of α-connexin carboxyl-terminal (aCT1) peptide in resistant HER2+ breast cancer

Project description: This study aims to examine the mechanisms for the anti-cancer effects of a therapeutic peptide agent targeted to connexin 43 (Cx43) called alpha-connexin carboxyl-terminal peptide (aCT1). Findings from this study identify the effect of aCT1 on breast cancer signaling using a resistant HER2+ breast cancer cell line.

2023-12-20 | GSE250543 | 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

Phenyl acid formation during mesophilic AD

Project description:Proteinaceous substrates lead to phenyl acid formation during mesophilic AD

| PRJNA564060 | ENA

Phenyl acid formation during thermophilic AD

Project description:Proteinaceous substrates lead to phenyl acid formation during thermophilic AD

| PRJNA564063 | ENA

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

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