Sertoli cell specific testicular gene expression of Connexin 43 knockout mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE23431 | GEO | 2011/01/06
SECONDARY ACCESSION(S): PRJNA131099
REPOSITORIES: GEO
Similar Datasets
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
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
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
Project description:Objectives: We studied the signal transduction of atrial structural remodelling that contributes to the pathogenesis of atrial fibrillation (AF). Backround: Fibrosis is a hallmark of arrhythmogenic structural remodelling but the underlying molecular mechanisms are incompletely understood. Methods: We performed transcriptional profiling of left atrial myocardium (LA) from patients with AF and sinus rhythm (SR) and applied cultured primary cardiac cells and transgenic mice with overexpression of constitutively active V12Rac1 (RacET) who develop AF at old age to characterize mediators of the signal transduction of atrial remodeling. Results: LA from patients with AF showed a marked upregulation of connective tissue growth factor (CTGF) expression compared SR patients. This was associated with increased fibrosis, NADPH-oxidase-, Rac1- and RhoA activity, upregulation of N-cadherin and connexin 43 (Cx43) expression and increased angiotensin II tissue concentration. In neonatal rat cardiac myocytes and -fibroblasts, a specific small molecule inhibitor of Rac1 or simvastatin completely prevented the angiotensin II induced upregulation of CTGF, Cx43 and N-cadherin expression. Transfection with small-inhibiting CTGF RNA blocked Cx43 and N-cadherin expression. RacET mice showed upregulation of CTGF, Cx43 and N-cadherin protein expression. Inhibition of Rac1 by oral statin treatment prevented these effects, identifying Rac1 as a key regulator of CTGF in vivo. Conclusion: The data identify CTGF as an important mediator of atrial structural remodelling during AF. Angiotensin II activates CTGF via activation of Rac1 and NADPH oxidase, leading to upregulation of Cx43, N-cadherin and interstitial fibrosis and therefore contributing to the signal transduction of atrial structural remodelling. Array design study consists of 5 Atrial Fibrillation patients and matched 5 samples of patients in sinus rhythm (controls).
2010-02-21 | E-GEOD-14975 | biostudies-arrayexpress
Project description:The atypical chemokine receptor 3 (ACKR3) plays a pivotal role in directing the migration of various cellular populations and its over-expression in various tumors promotes cell proliferation and invasiveness. The intracellular cellular pathways transducing ACKR3-dependent effects remain poorly characterized, an issue we addressed by characterizing the the interactome of recombinant ACKR3 expressed in HEK293T cells. Among the ACKR3-interacting proteins identified, we focused on the gap junction protein Connexin 43 (Cx43).
2020-07-07 | PXD016978 | Pride
Project description:<p>Osteocytes could release some small molecules (≤ 1 kDa) through gap junctions and hemichannels to extracellular environment, such as prostaglandin E2 (PGE2), nitric oxide (NO) and adenosine triphosphate (ATP), which play key roles in transferring signals between bone cells and other tissue cells. Connexin (Cx) 43 is the most abundant connexin in osteocytes. To further discover molecules released by osteocytes through Cx43 channels and better understand the regulatory function of Cx43 channels in osteocytes, we performed non-targeted global metabolomics analysis using liquid chromatography-tandem mass spectrometry (LC-MS/MS) on conditioned medium collected from osteocytes isolated from two transgenic mouse models with Cx43 dominant negative mutants driven by a 10 kb-DMP1 promoter: R76W (gap junctions are blocked, whereas hemichannels are promoted) and Δ130-136 (both gap junctions and hemichannels are blocked). The results revealed that several new categories of molecules, such as “fatty acyls” and “carboxylic acids and derivatives”, could be released through osteocytic Cx43 channels. In addition, alteration of Cx43 channel function affected the release of metabolites related to inflammatory reaction and oxidative stress. Pathway analysis further showed that citric acid cycle was the most differential metabolic pathway regulated by Cx43 channels. In sum, these results isolated new potential metabolites released by osteocytes through Cx43 channels, and offered a novel perspective to understand the regulatory mechanisms of osteocytes on themselves and other cells as well.</p>
2021-04-14 | MTBLS2358 | MetaboLights
Project description:Oocyte quality is a well- established determinant of embryonic fate. However, the molecular participants and biological markers that affect and predict adequate embryonic development are largely elusive. We have previously reported that oocyte- directed Connexin 43 (Cx43) depletion leads to embryo implantation defects, although both the morphology of the oocyte and processes presiding embryo implantation appear to undergo normally. In the context of previous data determining Cx43 indispensability to oocyte and embryonic development, we show here that the timing of Cx43 depletion from the oocyte and the ovarian follicle is crucial in determining the severity of subsequent embryonic defects. Specifically, we show that the implantation defects of blastocysts resulting from oocyte- directed Cx43- depleted follicles (depletion occurs at day 3 postnatal), is not due to maternal luteal insufficiency but rather depends solely on the defective blastocysts. Gene expression microarray analysis revealed global defects in the expression of ribosomal proteins, translation initiation factors and other genes associated with cellular biosynthetic and metabolic processes in these defective oocytes and specifically blastocysts. We therefore propose that timely expression of Cx43 in the oocyte and ovarian follicles is a major determinant of oocyte developmental competence, by determining the ability of the resulting blastocyst to facilitate biomass expansion and undergo adequate embryo implantation To study the effect of CX43 on the transcriptom of the pre implantation stages, we compared CX43 KO oocytes to the WT oocytes in three different stages of the very early development. First comparison MII oocytes, second comparison blastocysts, third comparison implantation site.
2013-01-01 | E-GEOD-35299 | biostudies-arrayexpress
Project description:Myofibroblasts (MFs) are crucial components of the fibrotic remodeling after myocardial infarction (MI). We have previously demonstrated the centrality of AMPKα1 in post-MI remodeling. Here, we investigate the effects of MF-specific deletion of AMPKα1 on left ventricular (LV) adaptation following MI, and the underlying molecular mechanisms. Importantly, MF-restricted AMPKα1 conditional knockout (cKO) hearts exhibit exacerbated post-MI adverse LV remodeling and are characterized by exaggerated fibrotic response, compared to wild-type (WT) hearts. Myofibroblast proliferation significantly increases in cKO infarcted hearts, coincident with a significant reduction of Connexin 43 (Cx43) expression in MFs. Mechanistically, lack of AMPKα1 in MFs enhances miR-125b expression, which, in turn, downregulates Cx43. Collectively, our data demonstrate a cardinal role for MF-AMPKα1 in cardiac remodeling, as its lineage-specific inactivation accentuates fibrosis and LV dilatation following MI. The deleterious effects of MF-specific AMPKα1 deletion are mediated via Cx43, and its post-transcriptional regulation by miR-125b.
2020-03-25 | GSE147470 | GEO
Project description:Objectives: We studied the signal transduction of atrial structural remodelling that contributes to the pathogenesis of atrial fibrillation (AF). Backround: Fibrosis is a hallmark of arrhythmogenic structural remodelling but the underlying molecular mechanisms are incompletely understood. Methods: We performed transcriptional profiling of left atrial myocardium (LA) from patients with AF and sinus rhythm (SR) and applied cultured primary cardiac cells and transgenic mice with overexpression of constitutively active V12Rac1 (RacET) who develop AF at old age to characterize mediators of the signal transduction of atrial remodeling. Results: LA from patients with AF showed a marked upregulation of connective tissue growth factor (CTGF) expression compared SR patients. This was associated with increased fibrosis, NADPH-oxidase-, Rac1- and RhoA activity, upregulation of N-cadherin and connexin 43 (Cx43) expression and increased angiotensin II tissue concentration. In neonatal rat cardiac myocytes and -fibroblasts, a specific small molecule inhibitor of Rac1 or simvastatin completely prevented the angiotensin II induced upregulation of CTGF, Cx43 and N-cadherin expression. Transfection with small-inhibiting CTGF RNA blocked Cx43 and N-cadherin expression. RacET mice showed upregulation of CTGF, Cx43 and N-cadherin protein expression. Inhibition of Rac1 by oral statin treatment prevented these effects, identifying Rac1 as a key regulator of CTGF in vivo. Conclusion: The data identify CTGF as an important mediator of atrial structural remodelling during AF. Angiotensin II activates CTGF via activation of Rac1 and NADPH oxidase, leading to upregulation of Cx43, N-cadherin and interstitial fibrosis and therefore contributing to the signal transduction of atrial structural remodelling.
2010-02-11 | GSE14975 | GEO
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