Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

EIF4G2-dependent translation of pro-fibrotic mRNAs is essential for cardiac fibroblast activation (Polysome-Seq)

ABSTRACT: eIF4G2-dependent translation of pro-fibrotic mRNAs is essential for cardiac fibroblast activation (Polysome-Seq)

PROVIDER: PRJNA1001024 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

eIF4G2-dependent translation of pro-fibrotic mRNAs is essential for cardiac fibroblast activation (Polysome-Seq)

Project description:RNA-binding proteins control gene expression in cardiac fibroblasts during TGFb-driven fibrotic responses, including the eukaryotic translation initiation factor 4G2 (eIF4G2), which was known to facilitate alternative mRNA translation during cellular stresses. However, the precise role of eIF4G2 in cardiac fibroblast activation in response to fibrotic stress remains unclear. In this study, we found increased eIF4G2 protein levels in the hearts of heart failure patients and myocardial infarcted mice, as well as in TGFb-treated immortalized human and primary mouse cardiac fibroblasts. Depletion of eIF4G2 led to predominant translational downregulation of genes that are enriched in focal adhesion and extracellular matrix pathways. eIF4G2 knockdown reduced the proliferation, migration, and collagen secretion of TGFb-treated cardiac fibroblasts. Mechanistically, we found that the translation of IGFBP7 mRNA relies on eIF4G2, which is crucial for ECM production in response to pro-fibrotic stimuli. The interaction between eIF4G2 and a DEAD box RNA helicase DDX24 can regulate IGFBP7 protein expression in cardiac fibroblasts. Together, these findings suggest that the TGFb-eIF4G2-IGFBP7 axis establishes a novel translational regulatory circuit that governs cardiac fibroblast activation. Furthermore, conditional knockout of Eif4g2 in POSTN-positive myofibroblasts reduced cardiac fibrosis in the myocardial infarction mouse model, thus improving cardiac function. Our study provides insights into the molecular mechanism of eIF4G2-mediated translational regulation of crucial physiological mRNAs during cardiac fibroblast activation.

2024-07-31 | GSE239823 | GEO

eIF4G2-dependent translation of pro-fibrotic mRNAs is essential for cardiac fibroblast activation (RIP-Seq)

2024-07-31 | GSE239824 | GEO

eIF4G2-dependent translation of pro-fibrotic mRNAs is essential for cardiac fibroblast activation

Project description:eIF4G2-dependent translation of pro-fibrotic mRNAs is essential for cardiac fibroblast activation

| PRJNA1001020 | ENA

eIF4G2-dependent translation of pro-fibrotic mRNAs is essential for cardiac fibroblast activation (RIP-Seq)

Project description:eIF4G2-dependent translation of pro-fibrotic mRNAs is essential for cardiac fibroblast activation (RIP-Seq)

| PRJNA1001026 | ENA

eIF4G2-dependent translation of pro-fibrotic mRNAs is essential for cardiac fibroblast activation

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

2024-07-31 | GSE239826 | GEO

Systemic pro-fibrotic and pro-inflammatory response in patients with advanced cirrhosis

Project description:Objective: To evaluate gene expression profiles in patients with advanced cirrhosis compared with healthy controls (HC). Results: Patients with advanced cirrhosis exhibit an unbalanced systemic response involving pro-fibrotic / protective signatures that could be contributing to the pathogenesis of cirrhosis and also to that of the extra-hepatic complications of this disease.

2016-02-14 | E-MTAB-3338 | biostudies-arrayexpress

Macrophage epoxygenase determines a pro-fibrotic transcriptomesignature

Project description:Epoxygenases belong to the cytochrome P450 family and they generate epoxyeicosatrienoic acids (EETs) known to have anti-inflammatory effects but little is known about their role in macrophage function. By high-throughput sequencing of RNA (RNA-seq) in primary macrophages derived fromrodents and humans, we establish the relative expression of epoxygenases in these cells. Zinc-finger nuclease-mediated targeted gene deletion of the major rat macrophage epoxygenase Cyp2j4 (orthologue of human CYP2J2),resulted inreduced EET synthesis. Cyp2j4-/-macrophages have relatively increased PPARγ levels and show a pro-fibrotic transcriptome,displayingover-expression of a specific subset of genes (260 transcripts) primarily involved in extracellular matrix, with fibronectin being the most abundantly expressed transcript.Fibronectin expression is under the control of epoxygenase activity in human and rat primary macrophages. In keeping with the invitro findings, Cyp2j4-/- rats show up-regulation of type I collagen following unilateral ureter obstruction (UUO) of the kidney and quantitative proteomics analysis (LC-MS/MS) showed increased renal type I collagen and fibronectin protein abundance resulting from experimentally induced crescentic glomerulonephritis in these rats. Taken together, these results identify the rat epoxygenase Cyp2j4 as a determinant of a pro-fibrotic macrophage transcriptome that could have implications in various inflammatory conditions depending on macrophage function. Gene expression profile generated for macrophages in wild type and Cyp2j4 KO WKY rats

2015-02-10 | E-GEOD-65715 | biostudies-arrayexpress

CCD18co colonic fibroblast cell line treated with various pro-inflammatory stimuli, and analized by single cell RNA sequencing (scRNA-seq) to analyze pro-fibrotic signatures

Project description:CCD18co cells are representative of colonic human fibroblasts. We wanted to understand if there was a stimulus that could induce the cells to acquire the same pro-fibrotic signatures that are found in patients with Ulcerative Colitis or Crohn's Disease. We stimulated the cells with various pro-fibrotic stimuli, and analyzed the signatures by single cell RNA sequencing (scRNA-seq)

2023-05-21 | GSE233063 | GEO

Myeloid cell analysis during a pro-fibrotic ischemia-reperfusion and cardiotoxin muscle injury.

Project description:Myeloid cells are critical to the development of fibrosis following muscle injury, however, the mechanism of their role in fibrosis formation remains unclear. Here we demonstrate that myeloid cell-derived TGF-β1 signaling is increased in a pro-fibrotic ischemia-reperfusion and cardiotoxin (IR/CTX) muscle injury model. This study analyzes scRNAsequencing from the fibrotic region after a pro-fibrotic ischemia-reperfusion and cardiotoxin muscle injury.

2020-01-28 | GSE144270 | GEO

YAP mediates TNF effect on pro-fibrotic genes expression

Project description:YAP mediates TNF effect on pro-fibrotic genes expression

| PRJNA799310 | ENA