Effect of hypoxia and TGFβ1 on gene expression in HPF fibroblast cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE139963 | GEO | 2019/11/06
REPOSITORIES: GEO
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Project description:Effect of hypoxia and TGFβ1 on gene expression in HPF fibroblast cells
| PRJNA587746 | ENA
Project description:Idiopathic pulmonary fibrosis is a chronic devastating disease of unknown etiology. No therapy is currently available. A growing body of evidence supports the role of TGFβ1 as the major player in the pathogenesis of the disease. This study designed novel human- and mouse-specific siRNAs and siRNA/DNA chimeras targeting both human and mouse common sequences and evaluated their inhibitory activity in pulmonary fibrosis induced by bleomycin and lung-specific transgenic expression of human TGFβ1. Selective novel sequences of siRNA and siRNA/DNA chimeras efficiently inhibited pulmonary fibrosis, indicating their applicability as tools for treating fibrotic disease in humans. Total RNA was extracted from lung tissue from mice with bleomycin (BLM)-induced lung fibrosis treated with mouse TGFβ1 siRNAs or vehicle on different days after BLM infusion.
2011-11-22 | E-GEOD-28122 | biostudies-arrayexpress
Project description:To verify whether ezetimibe inhibits myofibroblast differentiation at the transcriptome level and to reveal the mechanism of action of ezetimibe, we sequenced primary human lung fibroblasts that we isolated and cultured.
2024-02-22 | GSE225982 | GEO
Project description:4 replicates were prepared from A2058 melanoma cells [transfected with 10ng of empty vector (pcDNA3.1+)] and treated with 5ng/ml TGFβ1 or vehicle control for 24hrs This is the control arm of a larger experiment where cells transfected with a particular expression plasmid were treated with TGFβ1 or control vehicle. The transfection with the expresion plasmid was unsucessful so this empty vector data has been used alone to simply examine the effect of TGFβ1 treatment on A2058 cells.
2015-02-20 | E-GEOD-66114 | biostudies-arrayexpress
Project description:TGFβ1 is a profibrotic mediator that contributes to a broad spectrum of pathologies, including pulmonary fibrosis (PF). However, the secretome of TGFβ1-stimulated primary human normal lung (NL) fibroblasts has not been well characterized. Using fluorescent 2-dimensional gel electrophoresis (2D-PAGE) and differential gel electrophoresis (DIGE), we identified 37 differentially secreted proteins in the conditioned media of TGFβ1-activated NL fibroblasts and generated a protein-protein association network of the TGFβ1 secretome using STRING. Functional enrichment revealed that biological processes and pathways characteristics of PF were enriched. Using the DrugBank database, we determined that 32 of the secreted proteins are targets of known experimental, investigational and approved drugs. Additionally, by comparing the TGFβ1 secretome of NL fibroblasts to proteomic biomarkers from biological fluids of systemic sclerosis (SSc) patients, we identified 11 overlapping proteins. Together our data validate the TGFβ1-induced secretome of NL fibroblasts as a valid in vitro model that reflects SSc biomarkers and identifies potential therapeutic targets for SSc-PF.
2022-08-12 | PXD023862 | Pride
Project description:Intratumoral hypoxia causes the formation of dysfunctional blood vessels which contribute to tumor metastasis. Blood vessels are embedded in the tumor stroma where cancer-associated fibroblasts (CAFs) constitute the most prominent cellular component. We found that hypoxic human mammary CAFs promote blood vessel growth in CAF-endothelial cell co-cultures in vitro. Mass spectrometry-based proteomic analysis of CAF secretome unravels how hypoxic CAFs contribute to blood vessel abnormalities by altering the secretion of a multitude of pro- and anti-angiogenic factors. Hypoxia induces pronounced remodeling of the CAF proteome, including proteins that have not been previously related to this process. Our study provides a map of unprecedented depth of hypoxia-induced molecular alterations in mammary CAFs that can be exploited to identify novel mechanisms that control hypoxic CAF functions.
2019-02-15 | PXD006535 | Pride
Project description:To examine the effect of TGFβ1 on prostatic stromal cells, we firstly isolated primary prostatic stromal cells from five benign prostatic hyperplasia sample. Then RNA sequencing and bioinformatics analysis were used to reveal important pathways and hub genes associated with TGFβ1 stimulation on PrSCs.
2022-06-29 | GSE205378 | GEO
Project description:To further explore the effect of NAM on the TGFβ1-induced hESC-derived corneal endothelial progenitor cells, we have employed whole RNA microarray expression profiling as a discovery platform to identify genes and mechanism of NAM on the EnMT and senescence. hESC-derived endothelial progenotors were culured under 30ng/ml TGFβ1 with or without 50 mM NAM. The cultures were incubated for 72 hours at 37 ºC in a humidified incubator with 5% CO2.
2022-01-05 | GSE183786 | GEO
Project description:To determine whether RSPO1 and TGFβ1 activate similar transcription, RNA-seq analysis was performed to compare gene profiles after treatment by RSPO1 or TGFβ1. FET cells were treated with RSPO1 or TGFβ1 in triplicates for 4 hours and RNAs extracted from these cells were used for RNA-seq analysis. When gene expression profiles were compared, it was found that 153 genes were commonly regulated by either RSPO1 or TGFβ1. Interestingly, the majority of genes regulated by TGFβ1 were also regulated by RSPO1.
2017-09-09 | GSE103650 | GEO
Project description:T-helper 17 (Th17) cells play a dual role in immunological responses, serving as essential components in tissue homeostasis and host defense against microbial pathogens, while also contributing to proinflammatory conditions and autoimmunity. While Transforming Growth Factor-beta 1 (TGFβ1) is pivotal for the differentiation of non-pathogenic Th17 cells, the role of TGFβ3 and Activin in steering Th17 cells toward a pathogenic phenotype has been acknowledged. However, the molecular mechanisms governing this dichotomy remain elusive. In this study, we demonstrate that the transcription factor Foxo1 is upregulated in a TGFβ1 dose-dependent manner, serving as a critical regulator that specifically modulates the fate of pathogenic Th17 cells. Analyses in both uveitis patients and an Experimental Autoimmune Uveitis (EAU) mouse model reveal a strong correlation between disease severity and diminished Foxo1 expression levels. Ectopic expression of Foxo1 selectively attenuates IL-17A production under pathogenic Th17-inducing conditions. Moreover, enhanced Foxo1 expression, triggered by TGFβ1 signaling, is implicated in fatty acid metabolism pathways that favor non-pathogenic Th17 differentiation. Our drug screening identifies several FDA-approved compounds capable of upregulating Foxo1. Collectively, our findings offer compelling evidence that Foxo1 serves as a molecular switch to specifically control pathogenic versus non-pathogenic Th17 differentiation in a TGFβ1-dependent manner. These insights suggest that targeting Foxo1 could be a promising therapeutic strategy for autoimmune diseases, offering efficacy without compromising immune homeostasis.
2023-10-10 | GSE244599 | GEO