Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dysbacteriosis-induced LPS elevation disturbs the development of muscle progenitor cells by interfering with retinoic acid signaling

ABSTRACT: Dysbacteriosis-induced LPS elevation disturbs the development of muscle progenitor cells by interfering with retinoic acid signaling

PROVIDER: PRJNA580051 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Dysbacteriosis-induced LPS elevation disturbs the development of muscle progenitor cells by interfering with retinoic acid signaling [RNA-seq]

Project description:Dysbacteriosis-induced LPS elevation disturbs the development of muscle progenitor cells by interfering with retinoic acid signaling [RNA-seq]

| PRJNA580058 | ENA

Dysbacteriosis-induced LPS elevation disturbs the development of muscle progenitor cells by interfering with retinoic acid signaling [16S rRNA sequencing]

Project description:Dysbacteriosis-induced LPS elevation disturbs the development of muscle progenitor cells by interfering with retinoic acid signaling [16S rRNA sequencing]

| PRJNA579597 | ENA

Dysbacteriosis-induced LPS elevation disturbs the development of muscle progenitor cells by interfering with retinoic acid signaling [RNA-seq]

Project description:Whether myogenesis is affected by the maternal gut dysbacteriosis still remains ambiguous. In this study, firstly we show elevated level of lipopolysaccharides (LPS) in a gut microbiota dysbiosis mouse model. Secondly, we demonstrate that the diameter of muscle fibres, limb development and somitogenesis were inhibited in both gut microbiota dysbiosis and LPS exposed mice and chicken embryos. These might be due to LPS disturbed the cell survival and the key genes which regulating the somitogenesis and myogenesis. RNA sequencing and subsequent validation experiments verified that retinoic acid (RA) signaling perturbation was mainly responsible for the aberrant somite formation and differentiation. Subsequently, we found that LPS-induced Roxidative stress (ROS generation and antioxidant genes such as Nrf2, AKR) contributed to the above-mentioned interference with RA signaling. These findings highlight that the gut microbiota homeostasis also involved in regulating the development of muscle progenitor cells during pregnancy.

2020-05-08 | GSE139525 | GEO

Dysbacteriosis-induced LPS elevation disturbs the development of muscle progenitor cells by interfering with retinoic acid signaling [16S rRNA sequencing]

2020-05-08 | GSE139422 | GEO

Dysbacteriosis-induced LPS elevation disturbs the development of muscle progenitor cells by interfering with retinoic acid signaling

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-05-08 | GSE139526 | GEO

elevation soil samples

Project description:elevation soil samples Genome sequencing and assembly

| PRJNA917290 | ENA

Dysbacteriosis-Derived Lipopolysaccharide Causes Embryonic Osteopenia through Retinoic-Acid-Regulated DLX5 Expression.

Project description:Growing evidence suggests an adverse impact of gut microbiota dysbiosis on human health. However, it remains unclear whether embryonic osteogenesis is affected by maternal gut dysbacteriosis. In this study, we observed that elevated lipopolysaccharide (LPS) levels led to skeletal developmental retardation in an established mouse model of gut microbiota dysbiosis. Using chick embryos exposed to dysbacteriosis-derived LPS, we found restriction in the development of long bones as demonstrated by Alcian blue and alizarin red staining. Micro-CT and histological analysis exhibited decreased trabecular volume, bone mineral density, and collagen production, as well as suppressed osteoblastic gene expression (Ocn, Runx2, Osx, and Dlx5) in chick embryonic phalanges following LPS treatment. Atomic force microscopy manifested decreased roughness of MC3T3-E1 cells and poorly developed matrix vesicles (MVs) in presence of LPS. The expression of the aforementioned osteoblastic genes was suppressed in MC3T3-E1 cells as well. High-throughput RNA sequencing indicated that retinoic acid (RA) may play an important role in LPS-induced osteopenia. The addition of RA suppressed Dlx5 expression in MC3T3-E1 cells, as was also seen when exposed to LPS. Quantitative PCR, Western blot, and immunofluorescent staining showed that retinoic acid receptor α (RARα) was upregulated by LPS or RA treatment, while the expression of DLX5 was downregulated. CYP1B1 expression was increased by LPS treatment in MC3T3-E1 cells, which might be attributed to the increased inflammatory factors and subsequently activated NF-κB signaling. Eventually, blocking RA signals with AGN193109 successfully restored LPS-inhibited osteoblastic gene expression. Taken together, our data reveals that maternal gut microbiota dysbiosis can interfere with bone ossification, in which Dlx5 expression regulated by RA signaling plays an important role.

| S-EPMC7177785 | biostudies-literature

Overexpression of each of the 6 interfering TFs and 5 non-interfering TFs

2011-06-07 | GSE29728 | GEO

bacterial diversity along elevation gradient

Project description:bacterial diversity along elevation gradient Metagenome

| PRJNA906103 | ENA

Overexpression of each of the 6 interfering TFs and 5 non-interfering TFs

Project description:To clarify that the interfering effect in iPS induction was not because of extraordinary gene expression which was caused by overexpression of infected genes, transcriptional profile of the cells infected six genes were analysed using microarray analysis. As result, overexpression of each of the 6 interfering TFs in NSEB5-2C did not compromise transcriptional profile compared with the five non-interfering TFs. The cells were infected by retroviruses (carrying each ORF in pMXs-IRESNeo) at the titre in which around 95% of cells express the transgene. After 24hr of the infection, G418 was added to eliminate non-expressing cells. Each cells were harvested at 72hr after the infection.

2011-06-07 | E-GEOD-29728 | biostudies-arrayexpress

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