Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA1057238 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

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

Primary Osteocyte Supernatants Metabolomic Profiling of Two Transgenic Mice with Connexin43 Dominant Negative Mutants

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

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

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

Connexin 43 controls the immunoregulatory phenotype of astrocytes

Project description:Connexin 43 controls the immunoregulatory phenotype of astrocytes

| PRJNA434418 | ENA

Metabolic alterations of liver Connexin-43 knockout in mice

Project description:Metabolic alterations of liver Connexin-43 knockout in mice

| PRJEB40894 | ENA

Stimulation of the atypical chemokine receptor 3 inhibits connexin 43 gap junctional intercellular communication

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

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data