Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from bone marrow neutrophils with or without LPS stimulation in wild type and miR-125a deficient mice

ABSTRACT: Neutrophil activation plays a critical role in the inflammatory response to gram-negative bacterial infections. Lipopolysaccharide (LPS) from gram-negative bacterial has been shown to be a major mediator of neutrophil activation to produce pro-inflammatory cytokines, chemokines and ROS which are important to tissue damage in LPS induced septic shock. We used microarrays to detail the global gene expression of neutrophils from miR-125a+/+ and miR-125a-/- mice after LPS stimulation.

ORGANISM(S): Mus musculus

PROVIDER: GSE63739 | GEO | 2014/12/02

SECONDARY ACCESSION(S): PRJNA268949

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA-Seq of inflammatory stimulated HUVECs transfected with microRNA-125a-5p or negative control.

Project description:Purpose: In recent years, research has revealed the role of microRNAs (miRs) as important regulators of endothelial function. Notably, miR-125a is upregulated in the blood of patients with acute vascular diseases. Since miRNAs act out their function in networks, we aimed at investigating the presence of a miR-125a-related network regulating the endothelial barrier. Method: We investigated transcriptional changes of human umbilical cord endothelial cells (HUVEC) after miR-125a overexpression in an acute inflammatory in-vitro setting using Next Generation Sequencing. Briefly, primary HUVECs from five different donors were transfected either with hsa-miR-125a-5p or negative control (NC). After transfection HUVECs were cultivated for 18 hours and stimulated with TNF (25 ng/ml) for additional 6 hours. We compared the following groups: NC (18047-0001, 18047-0002, 18047-0003, 18047-0004, 18047-0005) versus miR125a: (18047-0006, 18047-0007, 18047-0008, 18047-0009, 18047-0010) Results: MiR-125a overexpression in inflammatory activated HUVECs significantly altered gene expression of 468 genes (FC: +1.25 to -1.25 p<0.01). We found eight potential miR-125a direct target genes involved in endothelial barrier function.

2022-02-07 | GSE196161 | GEO

MicroRNA-125a-5p overexpression in human macrophages

Project description:Systemic juvenile idiopathic arthritis (SJIA) is a severe childhood arthropathy with features of autoinflammation. Monocytes and macrophages in SJIA have a complex phenotype with both pro- and anti-inflammatory properties that combine features of several well characterized in vitro conditions used to activate macrophages. An important anti-inflammatory phenotype is expression of CD163, a scavenger receptor that sequesters toxic pro-inflammatory complexes that is highly expressed in both active SJIA and macrophage activation syndrome (MAS). CD163 is most strongly upregulated by IL-10 (M(IL-10)), and not by other conditions that reflect features seen in SJIA monocytes such as M(LPS+IC). MicroRNA play key roles balancing and integrating cellular signals such as those in macrophage polarization, and as such we hypothesize microRNA regulate macrophage functional responses in SJIA including CD163 expression in vitro. We find that two microRNA previously found to be elevated in active SJIA, miR-125a-5p and miR-181c, significantly reduced macrophage CD163 expression through two distinct mechanisms. Neither microRNA was elevated in M(IL-10) with robust CD163 expression, but were instead induced in M(LPS+IC) where they restricted CD163 mRNA expression. Mir-181 species directly targeted CD163 mRNA for degradation. In contrast, transcriptome analysis of miR-125a-5p overexpression identified “cytokine-cytokine receptor interactions” as the most significantly repressed gene pathway, including decreased IL10RA, which is required for IL-10-mediated CD163 expression. Finally, overexpression of miR-181c inhibited CD163 anti-inflammatory responses to hemoglobin or high mobility group box 1 complexes. Together, these data show that microRNA utilize multiple mechanisms to integrate well characterized polarization phenotypes and regulate macrophage functional properties seen in SJIA.

2018-04-12 | GSE104853 | GEO

Expression profiles of HSPCs overexpressing microRNA cluster 99b/let-7e/125a, miR-125a, miR-155 and empty vector.

Project description:Hematopoietic stem/progenitor cell (HSPC) traits differ between genetically distinct mouse strains. For example, DBA/2 mice have a higher HSPC frequency compared to C57BL/6 mice. We performed a genetic screen for microRNAs that are differentially expressed between LSK, LS−K+, erythroid and myeloid cells isolated from C57BL/6 and DBA/2 mice. This analysis identified 131 microRNAs that were differentially expressed between cell types and 15 that were differentially expressed between mouse strains. Of special interest was an evolutionary conserved miR-cluster located on chromosome 17 consisting of miR-99b, let-7e and miR-125a. All cluster members were most highly expressed in LSKs and down-regulated upon differentiation. In addition, these microRNAs were higher expressed in DBA/2 cells compared to C57BL/6 cells, and thus correlated with HSPC frequency. To functionally characterize these microRNAs, we overexpressed the entire miR-cluster 99b/let-7e/125a and miR-125a alone in BM cells from C57BL/6 mice. Overexpression of the miR-cluster or miR-125a dramatically increased day-35 CAFC activity and caused severe hematopoietic phenotypes upon transplantation. We showed that a single member of the miR-cluster, namely miR-125a, is responsible for the majority of the observed miR-cluster overexpression effects. Finally, we performed genome-wide gene expression arrays and identified candidate target genes through which miR-125a may modulate HSPC fate.

2011-12-15 | GSE33689 | GEO

Expression profiles of HSPCs overexpressing microRNA cluster 99b/let-7e/125a, miR-125a, miR-155 and empty vector.

2011-12-15 | E-GEOD-33689 | biostudies-arrayexpress

CodeLink Mouse Whole Genome Bioarray data from hematopoietic stem cells (HSCs) of miR-125a (+/+) wild-type and miR-125a knockout mice with myeloproliferative disorder (MPD)

2015-12-31 | GSE69621 | GEO

CodeLink Mouse Whole Genome Bioarray data from hematopoietic stem cells (HSCs) of miR-125a (+/+) wild-type and miR-125a knockout mice with myeloproliferative disorder (MPD)

Project description:miR-125a knockout mice develop myeloproliferative disorder (MPD). To investigate the molecular mechanisms of MPD induced by the loss of miR-125a, gene expression profiling on hematopoietic stem cells of miR-125a (+/+), (+/-) MPD, and (-/-) MPD mice was performed by using CodeLinkTM Whole Genome DNA array analysis. CodeLink Mouse Whole Genome Bioarrays were performed according to the manufacturerâs instruction on total RNA extracted from hematopoietic stem cells of miR-125a (+/+) wild-type mouse, miR-125a (+/-) heterozygous mouse with MPD, and miR-125a (-/-) homozygous mouse with MPD. One replicate per array.

2015-12-31 | E-GEOD-69621 | biostudies-arrayexpress

CodeLink™ Mouse Whole Genome Bioarray data from hematopoietic stem cells (HSCs) of miR-125a (+/+) wild-type mice and miR-125a (+/-) heterozygous mice with myeloproliferative disorder

2015-06-30 | GSE65648 | GEO

CodeLink™ Mouse Whole Genome Bioarray data from hematopoietic stem cells (HSCs) of miR-125a (+/+) wild-type mice and miR-125a (+/-) heterozygous mice with myeloproliferative disorder

Project description:miR-125a knockout mice develop myeloproliferave disorder (MPD). To investigate the molecular mechanisms of MPD induced by the loss of miR-125a, gene expression profiling on hematopoietic stem cells of miR-125a (+/+) and (+/-) MPD mice was performed using CodeLink Whole Genome DNA array analysis. Codelink Mouse Whole Genome Bioarrays were performed according to the manufacturer’s instruction on total RNA extracted from hematopoietic stem cells of miR-125a (+/+) wild-type mice and miR-125a (+/-) heterozygous mice with MPD. One replicate per array.

2015-06-30 | E-GEOD-65648 | biostudies-arrayexpress

Expression data on Treg cells isolated from wildtype mice and miR-125a deficient mice

Project description:We found miR-125a was a key regulator that stabilizes the commitment and immunoregulatory capacity of Treg cells.To gain insights into the general functional features of miR-125a-deficient Treg cells, we performed a genome-wide gene array analysis on Treg population isolated from the spleens of 6 to 8-week-old miR-125a-deficient and WT mice

2015-05-08 | GSE66608 | GEO

Gene expression analysis after miR-125a-3p over-expression in oligodendrocyte precursor cells (OPCs)

Project description:MiR-125a-3p over-expression in OPCs impairs their differentiation into fully mature oligodendrocytes. We performed a whole microarray profiling to identify new miR-125a-3p direct targets and altered signaling pathways responsible for its the detrimental effect on oligodendrocyte maturation.

2021-01-21 | GSE143876 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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