Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

EP2 receptor modulates macrophage activity for cardiac repair

ABSTRACT: EP2 receptor modulates macrophage activity for cardiac repair

PROVIDER: PRJNA480411 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

EP2 receptor modulates macrophage activity for cardiac repair

Project description:To examine the functional changes of macrophages isolated from wild-type or EP2-KO mice

2018-07-11 | GSE116848 | GEO

Targeting NPM1 Epigenetically Promotes Post-infarction Cardiac Repair by Reprogramming Reparative Macrophage Metabolism [RNA-Seq]

Project description:Background: Post-infarction heart failure is attributed to ischemia-induced myocardial inflammation and unfavorable remodeling, with reparative macrophages playing a crucial role in limiting excessive fibrosis and promoting cardiac repair via cytokine secretion and cross-cell interactions. Hence, a timely and adequate transition of macrophage phenotypes is essential for proper wound healing post-MI, but the precise mechanisms underlying this process remain incompletely elucidated. Methods: To elucidate the function of NPM1 in post-infarct cardiac repair, we generated macrophage-specific NPM1 knockout mouse models. Additionally, Cut&Tag assays were conducted on cardiac macrophages for the first time to explore the epigenetic mechanisms underlying NPM1-mediated regulation of macrophage metabolic reprogramming. Results: Macrophage-specific deletion of NPM1 in MI mouse models resulted in reduced tissue fibrosis and enhanced cardiac repair by promoting the phenotypic transition of macrophages towards a reparative state. NPM1 deletion also led to a shift in macrophage metabolism from glycolysis to mitochondrial OXPHOS via inactivation of the mTOR cascades. Mechanistically, we demonstrated that IL-4 induced NPM1 oligomerization, which recruited histone demethylase KDM5b to the promoter region of Tsc1, ultimately leading to macrophage metabolic rewiring. Antisense oligonucleotides and inhibitory compounds targeting NPM1 exhibited notable protective effects on cardiac repair post-MI. Conclusions: Our study demonstrates that NPM1 may serve as a promising prognostic biomarker and a valuable therapeutic target for ischemia-induced heart failure, shedding new light on the understanding of post-infarct cardiac repair and may pave the way for the development of innovative therapeutic strategies.

2026-01-26 | GSE230944 | GEO

Targeting NPM1 Epigenetically Promotes Post-infarction Cardiac Repair by Reprogramming Reparative Macrophage Metabolism [CUT&Tag]

2026-01-26 | GSE230938 | GEO

Meteorin-like regulates cardiac repair via macrophage modulation following myocardial infarction

Project description:After myocardial infarction (MI), the heart undergoes a reparative process that includes an initial acute inflammatory phase followed by a subsequent reparative phase. The transition between these phases is crucial for cardiac recovery, but the key factors remain unclear. Meteorin-like (Metrnl) promotes anti-inflammatory macrophage polarization in the myocardium, yet its role in the acute phase post-MI is unknown. We observed that macrophages infiltrating the ischemic myocardium produced elevated levels of Metrnl in both the heart and circulation 4 days post-MI. The absence of Metrnl in Metrnl⁻/⁻ mice altered myocardial healing and remodeling, with an increased presence of macrophages with a more pro-inflammatory phenotype. Conversely, cardiac Metrnl overexpression restored myocardial repair and promoted a shift toward a more anti-inflammatory macrophage phenotype. Mechanistically, Metrnl regulated macrophage-dependent production of Oncostatin M (Osm), a key cytokine in the early inflammatory phase post- MI that induces cardiomyocyte production of Reg3β. Reg3β, in turn, limits classical macrophage activation and polarization while modulating their trafficking, ultimately influencing the duration and intensity of the pro-inflammatory phase post-MI. Thus, Metrnl plays a crucial role in cardiac repair by modulating the acute phase following myocardial infarction through its regulation of macrophage populations.

2026-08-03 | GSE335342 | GEO

Meteorin-like regulates cardiac repair via macrophage modulation following myocardial infarction

Project description:Meteorin-like regulates cardiac repair via macrophage modulation following myocardial infarction

| PRJNA1477962 | ENA

Single-cell multiomic analysis identifies macrophage subpopulations in promoting cardiac repair

Project description:Single-cell multiomic analysis identifies macrophage subpopulations in promoting cardiac repair

| PRJNA1099260 | ENA

Single-cell multiomic analysis identifies macrophage subpopulations in promoting cardiac repair

Project description:Single-cell multiomic analysis identifies macrophage subpopulations in promoting cardiac repair

| PRJNA936797 | ENA

Single-cell multiomic analysis identifies macrophage subpopulations in promoting cardiac repair

Project description:Single-cell multiomic analysis identifies macrophage subpopulations in promoting cardiac repair

| PRJNA985639 | ENA

CIS Modulates Macrophage function

Project description:CIS Modulates Macrophage function

| PRJNA1402401 | ENA

MCG 101 tumors implanted on prostaglandin receptor EP2 wildtype and EP2 knockout mice

Project description:Wild type tumor cells, producing high levels of prostaglandin E2 (MCG101, EP2 +/+), were inoculated on EP2 knockout (EP2 -/-) and EP2 wild type (EP2 +/+) mice. Solid tumors were dissected into tumor- and tumor-stroma tissue compartments for RNA expression microarray screening, followed by metabolic pathway analyses. The study aims to evaluate simultaneous gene pathway expressions in separate tissue compartments, such as isolated tumor tissue and tumor stroma respectively.

2022-05-25 | GSE193098 | 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