Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from the cardiac tissue of Wild Type (WT) and ACKR4-knockout (ACKR4-KO) mice

ABSTRACT: Purpose:Atypical classical chemokine receptor 4 (ACKR4) is a newly reported atypical classical chemokine receptor. However, its expression and role in MI are still unknown. This study aims to determine whether ACKR4 modulates cardiac remodeling following MI and to explore the specific molecular mechanism. Methods: RNA sequencing of infarcted hearts from WT and ACKR4-KO mice was performed at day 14 post-MI. Results: We generated a library of distinct transcriptome expression patterns.The consistency in the clustering suggested a homogeneous genomic activity with limited background signal and high levels of reproducibility across the three biological replicates in each group.Utilizing a P value < 0.05 and fold changes of 1.5 or greater, we identified 774 genes that are differentially expressed in ACKR4-KO mice compared to WT mice.The downregulated-genes belonged to the GO classes taxis, chemotaxis, extracellular matrix, and cytokine activity. Conclusions: These data provide the first insight into the role and mechanism of ACKR4 in MI.

ORGANISM(S): Mus musculus

PROVIDER: GSE161415 | GEO | 2021/02/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression signatures of splenic CD31+ACKR4+ and CD31+ACKR4- endothelial cells from Ackr4GFP/wt mice

Project description:The atypical chemokine receptor 4 (ACKR4)-expressing spleen endothelial cells (ECs) form a three-dimensional sinusoidal network connected via shunts to the marginal sinus and tightly surrounds the outer perimeter of the marginal zone. To better define this new vascular compartment within the red pulp of the spleen, were sorted CD31+ACKR4+ and CD31+ACKR4- EC populations, routinely yielding 92-98% cell purity and analyzed their transcriptional profiles.

2022-03-01 | GSE171335 | GEO

Exome Sequencing of Ackr4-deficient mice in generation 12 (backcrossing to C57BL/6)

Project description:Purpose: The goal of this study was to compare exome sequences of Ackr4-deficient mice with C57BL/6 wildtype sequences to understand phenotypic differences which can not be explained by Ackr4-deficiency. Methods: Tail DNA of one wild-type (WT, C57BL/6) and atypical chemokine receptor 4 knockout (Ackr4−/−) mice was sequenced by exome sequencing using an Illumina NovaSeq 6000 sequencing system (2x 100bp). After demultiplexing (Illumina bcl2fastq 2.19) and adapter trimming (Skewer, 0.2.2), the trimmed reads were aligned with to the murine genome (mm10) with Burrows-Wheeler Aligner (BWA-mem 0.7.2-cegat). Reads aligned to multiple sides with the same mapping score were discarded. Further, duplicated reads were removed with SAMtool 0.1.18. Genetic variants were identified with Verscan 2.4.2-cegat and variants with a frequency of ≥ 2% were annotated with SnpEff (version 4.2 with GRCm38.75). Results: 100,000 to 140,000 million sequence reads per mouse were mapped to the mouse genome (build mm10). Each mouse had approx. 20,000 variants (insertions, deletions, SNPs) compared to the reference genome. In Ackr4-/- mice, 3,367 variants were present in both mice analysed, yet not detected in the C57BL/6 mouse used as control. 1781 of these 'shared' variants were present on the chromosome with the targeted Ackr4 allele (Chr9) and predominantly in close proximity to the Ackr4 locus, indicating that these variants originate from the 129-genetic background which was used for targeted mutagenesis during the generation of these mice. Conclusions: Our study shows that Ackr4-/- mice in generation F12 after backcrossing to the C57BL/6 background are still congenic for 129-derived DNA around the targeted Ackr4 locus, indicating that passenger mutations can influence the phenotype of these mice.

2019-12-21 | GSE138124 | GEO

Gene expression signatures of splenic CD31+ACKR4+ and CD31+ACKR4- endothelial cells from Ackr4GFP/wt mice

Project description:Gene expression signatures of splenic CD31+ACKR4+ and CD31+ACKR4- endothelial cells from Ackr4GFP/wt mice

| PRJNA719149 | ENA

Expression data from distinct populations of iMC from the small intestine of Ackr4(+/gfp) mice

Project description:Mesenchymal cells play key roles in modulating tissue homeostasis in various organs, including the intestine. Here we show that the murine intestinal mesenchymal cells are heterogenous, comprising at least three distinct populations. In this dataset, we include the expression data obtained from sorted subsets of CD45-Ter119-EPCAM-GP38+CD31- murine intestinal mesenchymal cell (iMC) populations. The iMC populations were separated into: CD146+ cells, which expressed CD9 and CD29, but not Ackr4, SCA1, ICAM1 or PDGFRa; GFP+ fibroblasts, which expressed Ackr4, SCA1, ICAM1 and PDGFRa; and GFP- fibroblasts, which also expressed SCA1, ICAM1 and PDGFRa, but were negative for Ackr4 expression.

2018-04-26 | GSE113665 | GEO

Gene expression analysis of in vitro activated B cells from C57BL/6 and Ackr4-deficient mice

Project description:To further understand differential phenotypes between C57BL/6 and Ackr4-deficient B cells, we have employed whole genome microarray expression profiling as a discovery platform to identify genes which are differentially expressed in the two genotypes. Murine B cells from spleens of C57BL/6 and Ackr4-deficient mice were purified by negative magnetic activated cell sorting (MACS) and activated in vitro with 10 µg/mL polyclonal anti-IgM and10 µg/mL anti-CD40 (clone FGK4.5) antibodies for three days in culture (96well plate, 37°C, 5%CO2). On day three, living B cells were sorted and RNA was extracted.

2019-12-21 | GSE138175 | GEO

m6A mRNA modification is a rheostat to maintain colonic epithelial cell homeostasis [bulkRNA-seq]

Project description:The function of m6A modification in colonic epithelial cells has been validated in our study that depletion of METTL14 in colonic epithelial cells triggers cell death. To further explore the biological effects of m6A deficiency in colonic epithelial cells, we performed RNA sequencing analysis of colonic epithelial cells form 2-week-old Mettl14-KO and WT control mice.The bioinformatic analysis revealed that METTL14 depletion increased the mRNA expression of NF-kB inhibitor Nfkbia, which favored TNF-induced cell death.

2022-04-19 | GSE171421 | GEO

Mus musculus

Project description:Atypical chemokine receptor 1 controls haematopoiesis

| PRJNA341496 | ENA

Malaria-associated atypical memory B cells exhibit markedly reduced B cell receptor signaling and effector function

Project description:Plasmodium falciparum malaria is a deadly infectious disease for which we have no licensed vaccine. Antibodies confer protection against malaria and individuals exposed to P. falciparum acquire protective antibodies, but only after years of repeated infections. We recently showed that malaria exposure is associated with a large expansion of a population of atypical memory B cells (MBCs) that phenotypically resemble B cell populations expanded in chronic viral infections, including HIV. At present the relationship of atypical MBCs to classical MBCs and their function are not known. We provide evidence that the expressed VH gene repertoires and somatic hypermutation rates of atypical and classical MBCs are indistinguishable, indicating the two populations are closely related developmentally. Atypical MBCs can be distinguished by their expression of multiple inhibitory receptors, including Fc receptor-like-5. B cell receptor (BCR) signaling is stunted in atypical MBCs, resulting in impaired Ca2+ mobilization, proliferation and cytokine production. Atypical MBCs do not spontaneously secrete antibodies and cannot be stimulated to differentiate into antibody-secreting cells in vitro. These results suggest that in individuals chronically exposed to malaria, atypical MBCs differentiate from classical MBCs and assume a phenotype refractory to BCR-mediated activation, potentially contributing to the inefficient acquisition of immunity to malaria. Comparison of human atypical B cell versus classical B cell versus naïve B cell.

2015-05-07 | E-GEOD-65928 | biostudies-arrayexpress

Characterisation of the pseudokinase SCYL1

Project description:In the project “Characterisation of the pseudokinase SCYL1” by Stéphanie Kaeser-Pebernard and Jörn Dengjel, 3 sets of experiments were performed to study the function of SCYL1. (1) Classical affinity purification-MS of HA-SCYL1 expressing cells were performed to study the SCYL1 interactome. (2) Conditioned medium of SCYL1 KO, GORAB KO and WT MCF7 cells was analyzed to study potential effects of SCYL1 on the proteome of exosomes. (3) Expression proteomics of SCYL1 KO and WT MCF7 cells was performed.

2022-07-19 | PXD024550 | Pride

Dapagliflozin protects against chronic heart failure in mice via inhibiting macrophage-mediated inflammation, independent of SGLT2 [RNA-Seq]

Project description:The specific mechanism of sodium-glucose cotransporter 2 (SGLT2) inhibitor in heart failure (HF) needs to be elucidated. In this study, we use SGLT2 global knockout (SGLT2-KO) mice to assess the mechanism of SGLT2 inhibitor on HF. Dapagliflozin ameliorates both myocardial infarction (MI)-and transverse aortic constriction (TAC) -induced HF. Global SGLT2-deficiency doesn’t exert protection against adverse remodeling in both MI- and TAC-induced HF models. Dapagliflozin blurs MI- and TAC-induced HF phenotypes in SGLT2-KO mice. Dapagliflozin causes major changes in cardiac fibrosis and inflammation. Based on single-cell RNA sequencing dapagliflozin causes significant differences in the gene expression profile of macrophages and fibroblasts. Moreover, dapagliflozin directly inhibites macrophage inflammation, thereby suppressing cardiac fibroblasts activation. The cardio-protection of dapagliflozin is blurred in mice treated with a C-C chemokine receptor type 2 (CCR2) antagonist. Taken together the protective effects of dapagliflozin against HF are independent of SGLT2, macrophage inhibition is the main target of dapagliflozin against HF.

2023-11-14 | GSE247062 | 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