Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA340782 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To identify the target gene repertoire of miRNAs (i.e. the miRNA-targetome) of unstimulated and TGF-β1-stimulated primary parenchymal lung fibroblasts, Ago2-IP was performed followed by mRNA expression profiling.
2017-11-01 | GSE86183 | GEO
Project description:miRNA expression data in unstimulated and TGF-β1-stimulated lung fibroblasts
| PRJNA340781 | ENA
Project description:To investigate the functional role of APOL2 in liver fibrosis, we performed an unbiased immunoprecipitation-mass spectrometry (IP-MS) analysis for APOL2 in the TGF-β1-stimulated LX-2 cell lysates.
2024-08-13 | PXD047815 | Pride
Project description:Here, we showed that baicalein suppressed transforming growth factor β1 (TGF β1)-stimulated the production of type I collagen in lung fibroblast MRC-5 cells. By applying SILAC-based proteomic technology, 158 proteins were identified as baicalein-modulated proteins in TGF β1-stimulated the accumulation of type I collagen in MRC-5 cells. Our proteomic and biochemical analysis demonstrated that baicalein could decrease the expression levels of connective tissue growth factor (CTGF) in TGF β1-stimulated MRC-5 cells. In addition, CTGF overexpression elevated the levels of type I collagen in baicalein-treated fibroblasts. Moreover, our results demonstrated that baicalein-downregulated CTGF expression might be related with the decrease of Smad2 phosphorylation, but not SP1.
2020-09-21 | PXD016167 | Pride
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
Project description:We performed Chromatin-Immunoprecipitation followed by Next-Generation Sequencing (ChIP-Seq) in PC-3 Cells stimulated with TGF-β1 for different duration. We used anti-H3K4me3 antibody to immunoprecipitate DNA fragment associated with H3K4me3. We found that a number of regions associated with H3K4me3 increased in a time-dependent manner upon TGF-β1 stimulation. Further the regions were classified into different Functional annotations.
2021-10-27 | GSE171058 | GEO
Project description:ABSTRACT Background: Primary human distal lung/parenchymal fibroblasts (DLF) exhibit a different phenotype from airway fibroblasts (AF), including the expression of high levels of alpha-SMA. The scope of the differences and the mechanisms driving them are unknown. We hypothesized that the distinct fibroblast characteristics based on lung region predicted a broad range of genomic differences which contribute to distinctly different functional pathway activation in AF and DLF. Methods and Findings: To investigate whether comprehensive gene expression patterns vary between AF and DLF, we compared global gene expression profiles of 3 matched pairs of primary human fibroblasts isolated from proximal and distal lung. 194 transcripts were upregulated in AF, and 290 transcripts upregulated in DLF. Quantitative real-time PCR (qRT-PCR) from both asthmatic and normal subjects confirmed the validity of microarray data (n = 8). Further analysis identified distinct pathway activation patterns, including the identification of the TGF-β receptor/SMAD3 signaling pathway as critical to the phenotypic differences in AF and DLF. The functional impact of these molecular differences on AF and DLF was then analyzed using Western blot, qRT-PCR, ELISA and gene knock-down approaches. TGF-β receptor/SMAD2-3 pathway analysis confirmed the contribution of higher TGF-β1 expression and accompanying SMAD3 and JNK activation to the increased alpha-SMA level seen in DLF. There are two limitations associated with our work. First, the microarray sample size was small. Second, for ethical reasons, a large majority of our data were from asthmatic subjects, only one pair of airway and distal lung tissues from a subject without knowing preexisting lung disease matched for age and smoking status was available. In this single normal subject, the same pattern of differences existed, supporting the concept that these genomic differences are regional, rather than disease-related. Conclusions: These findings demonstrated marked molecular and functional differences for these two lung regional fibroblast populations. These results suggest that airway and parenchymal fibroblasts differ in their responses to injury, repair, and remodeling in the lungs. There are likely profound implications of these observations for understanding mechanisms of development of fibrotic lung diseases as well as approaching therapy. In order to identify the underlying molecular differences between airway- and distal lung fibroblasts, microarray analysis was performed on 3 different matched pairs of fibroblasts.
2011-07-21 | E-GEOD-19362 | biostudies-arrayexpress
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
Project description:We generated single-cell RNA sequencing (scRNAseq) datasets of primary cultures of human proximal tubular cells stimulated with TGF-β1 or vehicle. Following TGF-β1 stimulation, hPTC expressed TGF-β1 and its downstream targets. Moreover, TGF-β1-treated hPTC were characterized by a differential expression of pro-fibrotic genes, which we had recently showed to be characteristic of polyploid hPTC and were enriched with hypertrophy, indicative of cell polyploidization.
2023-09-08 | GSE242695 | GEO
Project description:Fibrotic diseases have significant health impact and have been associated with differentiation of the resident fibroblasts into myofibroblasts. In particular, stiffened extracellular matrix and TGF-β1 in fibrotic lesions have been shown to promote pathogenic myofibroblast activation and progression of fibrosis in various tissues. To better understand the roles of mechanical and chemical cues on myofibroblast differentiation and how they may crosstalk, we cultured primary valvular interstitial cells (VICs) isolated from porcine aortic valves and studied how traditional TCPS culture, which presents a non-physiologically stiff environment, and TGF-β1 affect native VIC phenotypes. We carried out gene expression profiling using porcine genome microarrays from Affymetrix and found that traditional TCPS culture induces major changes in gene expression of native VICs, rendering these cells more activated and similar to cells treated with TGF-β1. We also monitored time-dependent effects induced by TGF-β1 by examining gene expression changes induced by TGF-β1 at 8 hours and 24 hours. Porcine aortic VICs were isolated and cultured with or without TGF-β1 treatment for RNA extraction and hybridization on Affymetrix microarrays. We included 3 biological replicates for each condition. P0 VICs were freshly isolated cells which had not been cultured. P2 VICs were cells that had been passaged 2 times and cultured on plastic plates in low serum media. Some of the P2 VICs were treated with TGF-β1 at 5ng/ml for 8 hours or 24 hours. All the control and TGF-β1-treated conditions were collected at the same time on day 3 of culture.
2013-09-02 | E-GEOD-48839 | biostudies-arrayexpress