Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-sequencing of primary mouse lung fibroblasts treated with TGF-β1

ABSTRACT: Fibroblast activation is accompanied by extensive transcriptional and metabolic remodeling that supports extracellular matrix production during pulmonary fibrosis. In this study, we investigated how palmitoleic acid, a lipid mediator generated by BAAMs through SCD1-dependent lipid remodeling, influences the transcriptional state of activated lung fibroblasts. Bulk RNA sequencing of primary mouse lung fibroblasts revealed coordinated upregulation of glycolytic pathways and suppression of oxidative phosphorylation and fatty-acid oxidation following fibroblast activation.

ORGANISM(S): Mus musculus

PROVIDER: GSE342858 | GEO | 2026/08/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Low input lipidomics analysis reveals remodeling of lipid metabolism and saturation during mouse and human preimplantation embryo development

Project description:Scd1 is responsible for forming a carbon-carbon double bound at the 9-10th position from the C-terminus of saturated fatty acids such as palmitic acid and stearic acid (C16:0 and C18:0), to generate the products of palmitoleic acid (C16:1) and oleic acid (C18:1).Here, we found SCD1 is required for in vitro blastocyst embryo development, and one of the mechanisms is through regulating unsaturated fatty acid-mediated membrane fluidity and formation of apical domain. Overall, our study provides invaluable resources for lipid reprogramming in mammalian preimplantation embryo development and mechanistic insights on regulation of embryogenesis by lipid unsaturation.

2023-10-19 | GSE213782 | GEO

miRNA expression data in unstimulated and TGF-β1-stimulated lung fibroblasts

Project description:Lung fibroblasts play an important role in extracellular matrix homeostasis and this process is mainly regulated by transforming growth factor-beta (TGF-β). Hence, lung fibroblasts are postulated to play a crucial role in aberrant lung tissue repair and remodeling, which is a main factor in lung diseases like COPD. In this study, the effect of TGF-β1 on the miRNA expression in parenchymal lung fibroblasts is investigated.

2017-11-01 | GSE86185 | GEO

Distinct phenotypes induced by acute hypoxia and TGF-β1 in human adult cardiac fibroblasts

Project description:Myocardial infarctions cause hypoxic injury to downstream tissue and a consequent fibrotic remodeling process to replace injured tissue with a scar. Scar formation occurs through phases of wound healing in which stimuli such as transforming growth factor-beta (TGF-β) drive cardiac fibroblasts to activate into a myofibroblast phenotype and deposit matrix molecules that form a scar. While this is necessary to repair injured tissue, excessive fibrosis commonly occurs which is correlated with heart failure. Therefore, defining cardiac fibroblast phenotypes under hypoxic stimuli and TGF-β is essential for understanding and treating pathological fibrosis. We robustly characterized fibroblast phenotype through immunofluorescence, quantitative RT-PCR, and proteomic analysis, after either TGF-β treatment or hypoxia durations that mimic acute hypoxic injury post-infarction. We find that hypoxic fibroblasts respond to low oxygen with increased hypoxia inducible factor 1 (HIF-1) but not HIF-2 activity by 4h. This is accompanied by increased gene and protein levels of VEGFA and LOX, respectively, which are both targets of HIF-1. Both TGF-β1 and hypoxia inhibit proliferation by 24h. While TGF-β1 treatment upregulated various fibrotic pathways, hypoxia causes a global reduction in protein synthesis, including collagen biosynthesis. This study discerns overlapping from distinctive outcomes of TGF-β1 and hypoxia treatment, which is important for elucidating their roles in fibrotic remodeling post-MI.

2024-07-03 | PXD051197 | Pride

Critical role for the TGF-β1/mTORC1 signalling axis in defining the transcriptional identity of CTHRC1+ pathologic fibroblasts in idiopathic pulmonary fibrosis

Project description:Fibroblasts represent key effector cells responsible for fibrogenesis during wound healing and pathological fibrosis, including idiopathic pulmonary fibrosis (IPF), the most rapidly progressive and fatal fibrotic lung disease. Single-cell RNA sequencing of fibrotic lung tissue has identified a novel population of high collagen-producing fibroblasts not present in non-diseased control lung, characterised by high expression of the marker, collagen triple helix repeat containing 1 (CTHRC1). The cardinal pro-fibrotic mediator TGF-β1 has been widely implicated in promoting fibrogenesis in multiple fibrotic conditions. In addition to the canonical Smad signalling pathway, TGF-β1-induced collagen I production is under critical regulatory control by the mTORC1/4E-BP1 signalling hub. Using pharmacological inhibition (dual ATP-competitive mTOR inhibitors and rapamycin) in combination with gene-editing approaches, we now demonstrate that the role of the mTORC1 axis extends to the regulation of over a third of all TGF-β1 regulated matrisome genes. We further show that the global transcriptome of TGF-β1-stimulated fibroblasts matches that of CTHRC1+ pathological fibroblast population in the IPF lung. In contrast, the TGF-β1 induced transcriptome of fibroblasts in which mTORC1-signalling is disrupted (by RPTOR gene editing using CRISPR-Cas9) does not map to any known fibroblast population. These data define, for the first time, a critical role for both TGF-β1 and the mTORC1 signalling hub in determining the transcriptional identity of CTHRC1+ pathological fibroblasts and provide strong scientific support for targeting mTORC1 as a therapeutic strategy in IPF and potentially other fibrotic conditions associated with dysregulated TGF-β1 profibrotic signalling.

2026-07-21 | GSE272972 | GEO

RNA-seq of human lung fibroblasts with and without TGF-beta1

Project description:Analysis of genes induced by TGF-beta1 in human lung fibroblasts. TGF-beta1 is essential for fibroblast -myofibroblast differentiation, which is a hallmark in the development of lung fibrosis. Newly identified genes up- or down-regulated by TGF-beta1 in human lung fibroblasts may serve as pharmacological target for therapeutic options in patients with lung fibrosis.

2022-04-14 | E-MTAB-11629 | biostudies-arrayexpress

Adipocyte associated glucocorticoid signaling regulates normal fibroblast function which is lost in inflammatory arthritis [fibroblast_bulk RNAseq]

Project description:Fibroblasts play critical roles in tissue homeostasis, but in pathologic states can drive fibrosis, inflammation, and tissue destruction. In the joint synovium, fibroblasts provide homeostatic maintenance and lubrication. Little is known about what regulates the homeostatic functions of fibroblasts in healthy conditions. We performed RNA sequencing of healthy human synovial tissue and identified a fibroblast gene expression program characterized by enhanced fatty acid metabolism and lipid transport. We found that fat-conditioned media reproduces key aspects of the lipid-related gene signature in cultured fibroblasts. Fractionation and mass spectrometry identified cortisol in driving the healthy fibroblast phenotype, confirmed using glucocorticoid receptor gene (NR3C1) deleted cells. Depletion of synovial adipocytes in mice resulted in loss of the healthy fibroblast phenotype and revealed adipocytes as a major contributor to active cortisol generation via Hsd11β1 expression. Cortisol signaling in fibroblasts mitigated matrix remodeling induced by TNFα- and TGFβ, while stimulation with these cytokines repressed cortisol signaling and adipogenesis. Together, these findings demonstrate the importance of adipocytes and cortisol signaling in driving the healthy synovial fibroblast state that is lost in disease.

2024-08-08 | GSE233501 | GEO

Adipocyte associated glucocorticoid signaling regulates normal fibroblast function which is lost in inflammatory arthritis [adipose_scRNAseq]

2024-08-08 | GSE233500 | GEO

Adipocyte associated glucocorticoid signaling regulates normal fibroblast function which is lost in inflammatory arthritis [synovium_scRNA-seq]

2024-08-08 | GSE233502 | GEO

A mRNA motif mediates TGF-β1 upregulation of NEU3 translation in human lung fibroblasts

Project description:To elucidate how TGF-β1 regulates translation, we treated human lung fibroblasts (HLF) with TGF-β1 and used RNA-seq to determine the effect of TGF-β1 on total RNAs, and mRNA polysome/monosome ratios.

2022-04-28 | GSE201506 | GEO

Transcriptomic profiling of TGF-β–stimulated primary mouse cardiac fibroblasts

Project description:Primary cardiac fibroblasts were isolated from neonatal C57BL/6J mouse hearts and stimulated with TGF-β1 in vitro to induce a profibrotic phenotype. Bulk RNA sequencing was performed on fibroblasts treated with TGF-β for 48 hours and on matched untreated controls to characterize transcriptional programs associated with TGF-β–driven fibroblast activation. Differential expression and gene ontology analyses were used to identify pathways related to extracellular matrix remodeling, TGF-β signaling, and DNA damage responses. These data support mechanistic studies on CRABP2–MRE11–MRN–dependent regulation of cardiac fibroblast activation and fibrosis.

2026-01-06 | GSE315365 | 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