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Links from GEO DataSets

Items: 20

1.

Global transcriptomic changes in human lung fibroblasts MRC5 exposed to conditioned media from RAS-activated alveolar epithelial type II (ATII) cells based on RNA-seq.

(Submitter supplied) IPF (idiopathic pulmonary fibrosis), a progressive lung disease with an unmet need for treatment, causes increased morbidity and mortality worldwide. Abnormal wound healing is strongly implicated in IPF, but the underlying mechanisms remain poorly understood. Here we reported that aberrant epithelial-mesenchymal crosstalk provides self-sustaining pro-fibrotic signals in IPF. By performing RNA-sequencing (RNA-seq) in human lung fibroblasts MRC5 treated with either conditioned media (CM) from control or 4-OHT (4-hydroxytamoxifen) - treated ATIIER:KRASV12 cells (kindly provided by Prof Julian Downward, The Francis Crick Institute, UK), in which addition of 4-OHT acutely activates RAS pathway (Yao et al. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: TXT
2.

Human alveolar epithelial cells (A549) exposed to cigarette smoke extract

(Submitter supplied) Human alveolar epithelial cells were exposed to cigarette smoke extract (CSE) for 1, 3 and 5 weeks at 1%, 5% and 10%, and gene expression was evaluated by complete transcriptome microarrays. In this study we explored the effect of cigarette smoke on the gene expression profile.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
36 Samples
Download data: CEL
Series
Accession:
GSE77942
ID:
200077942
3.

Gene expression data in over expressed Human Fetal Lung Fibroblasts with IPF downregulated miRNAs

(Submitter supplied) Idiopathic pulmonary fibrosis (IPF) is an untreatable fibrotic lung disease characterized by fibroblast proliferation and epithelial mesenchymal transition.miRNA let-7d and mir30b were found to be signifcantly down regulated in IPF. Compared to control we over expressed these miRNAs in Human Fetal Lung Fibroblast cell line
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6480
20 Samples
Download data: TXT
Series
Accession:
GSE38530
ID:
200038530
4.

Transcriptomic Profiling of Fibrosis-Specific Epithelial Cells in Idiopathic Pulmonary Fibrosis

(Submitter supplied) We aimed at characterizing disease-specific differences by comparing the transcriptomes of epithelial cells (ECs) from idiopathic pulmonary fibrosis (IPF) and non-IPF sources
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
10 Samples
Download data: CSV, RDS
Series
Accession:
GSE151673
ID:
200151673
5.

Feedback amplification of fibrosis through matrix stiffening and COX-2 suppression

(Submitter supplied) We tested the hypothesis that increasing matrix stiffness on which normal human lung fibroblasts are grown promotes the expression of a fibrogenic cellular transcriptomic program. Keywords: Human lung fibroblast, matrix stiffness, PTGS2, COX-2, Prostaglandin E2
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
15 Samples
Download data: CEL
Series
Accession:
GSE22011
ID:
200022011
6.

IPF versus Control

(Submitter supplied) Archived lung tissues of patients with IPF were obtained from the tissue bank of the Department of Pathology at the University of Pittsburgh. The diagnosis of IPF was confirmed by open lung biopsy. All patients fulfilled the criteria of the American Thoracic Society and European Respiratory Society for the diagnosis of IPF. Normal histology lung tissues resected from patients with lung cancer were used as controls. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS1252
Platform:
GPL1739
26 Samples
Download data
Series
Accession:
GSE2052
ID:
200002052
7.
Full record GDS1252

Idiopathic pulmonary fibrosis

Expression profiling of lung tissues from patients with idiopathic pulmonary fibrosis (IPF), a progressive and lethal disorder characterized by the abnormal formation of fibrous scar tissue in the lungs. Results provide insight into the pathogenesis of IPF.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 4 disease state sets
Platform:
GPL1739
Series:
GSE2052
26 Samples
Download data
8.

MMP1 and MMP7 as potential peripheral blood biomarkers in Idiopathic Pulmonary Fibrosis

(Submitter supplied) Idiopathic pulmonary fibrosis (IPF) is a chronic progressive fibrotic lung disease associated with significant morbidity and mortality. We identified a combinatorial signature of 5 proteins that was sufficient to distinguish IPF patients from controls; of these proteins MMP7 and MMP1 exhibited significantly higher values in both peripheral blood concentrations and lung tissue gene expression, suggesting their role as true biomarkers. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL4133
46 Samples
Download data: TXT
Series
Accession:
GSE10667
ID:
200010667
9.

Single Cell Analysis of Pulmonary Fibrotic Mesenchymal Cells Indicates a New Subtype

(Submitter supplied) Stromal taxonomy consists of multiple cell subtypes that play a critical role in tissue repair or regeneration, fibrosis, inflammation, angiogenesis and tumor formation. However, their identities are not fully understood, as these conventional classified populations have historically been defined by restricted sets of markers. We performed single-cell RNA sequencing to investigate stromal mesenchymal cells (MCs) in normal and fibrotic mouse lung. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
6 Samples
Download data: CSV, XLSX
Series
Accession:
GSE104154
ID:
200104154
10.

MiR-199a-5p determines fibroblast activation and pulmonary fibrogenesis

(Submitter supplied) Idiopathic pulmonary fibrosis (IPF) is a chronic and often fatal pulmonary disorder characterized by fibroblast proliferation and the excess deposit of extracellular matrix proteins. The etiology of IPF is unknown, but a central role for microRNAs (miRNAs), a class of small non-coding regulatory RNAs, has been recently suggested. We report the upregulation of miR-199a-5p in mouse lungs undergoing bleomycin-induced fibrosis and also in human biopsies from IPF patients. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array; Non-coding RNA profiling by array
Platforms:
GPL13607 GPL7686 GPL13912
48 Samples
Download data: GPR, TXT
Series
Accession:
GSE34818
ID:
200034818
11.

Impact of miR-199-5p overexpression and CAV1 silencing on human lung fibroblasts

(Submitter supplied) To identify putative novel specific targets of mir-199-5p, we overexpressed miR-199a-5p as well as miR-21 and a siRNA targeted against CAV1 in human HFL1 pulmonary fibroblasts (CCL-153) by transfecting them with synthetic pre-miRNAs or a synthetic “negative” pre-miRNA as control (miR-Neg). RNA samples were harvested at 48 hours post-transfection and 2 independent experiments were carried out. Additional samples correspond to HFL1 cells treated or not with 10ng/ml TGFbeta for 48 hours in the absence of serum (2 independent experiments).
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL13607
14 Samples
Download data: TXT
Series
Accession:
GSE34815
ID:
200034815
12.

mRNA reponse to bleomycin instillation

(Submitter supplied) Gene expression analysis of C57BL/6 mice challenged by intratracheal bleomycin instillation: mRNA expression profiles were established from lungs following a 14-days PBS or bleomycin administration.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL13912
10 Samples
Download data: TXT
Series
Accession:
GSE34814
ID:
200034814
13.

miRNA reponse to bleomycin instillation

(Submitter supplied) Comparison of C57BL/6 (sensitive) and BALB/c (resistant) mice challenged by intratracheal bleomycin instillation: miRNA expression profiles were established from lungs derived from the two strains, following a 7- or 14-days PBS or bleomycin administration.
Organism:
Mus musculus; Homo sapiens
Type:
Non-coding RNA profiling by array
Platform:
GPL7686
24 Samples
Download data: GPR
Series
Accession:
GSE34812
ID:
200034812
14.

Syndecan-1 promotes lung fibrosis by regulating epithelial reprogramming through extracellular vesicles (miRNA-Seq)

(Submitter supplied) We studied transcriptomic changes of extracellular vesicles (EVs) in bronchoalveolar lavage fluid of bleomycin-injured wild-type and syndecan-1 deficient mice
Organism:
Mus musculus
Type:
Non-coding RNA profiling by high throughput sequencing
Platform:
GPL17021
16 Samples
Download data: XLSX
Series
Accession:
GSE134948
ID:
200134948
15.

Syndecan-1 promotes lung fibrosis by regulating epithelial reprogramming through extracellular vesicles (RNA-Seq)

(Submitter supplied) We evaluted the effects of extracellular vesicles of bleomycin-injured wild-type and syndecan-1 deficient mice on mouse lung epithelial cell line (MLE-12) total transcriptomic changes (bulk mRNA sequencing)
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
9 Samples
Download data: XLSX
Series
Accession:
GSE134741
ID:
200134741
16.

mouse lung single cell RNA-seq

(Submitter supplied) Single cell RNA-seq profiling adult mouse lung cells reveal the cell heterogeneity and mechanism during lung fibrosis process.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: H5
Series
Accession:
GSE131800
ID:
200131800
17.

Single cell RNA-seq revealed critical genetic programs of invasive fibroblasts for pulmonary fibrosis

(Submitter supplied) We performed a single cell RNA-seq survey of 14,704 invasive fibroblasts and 16,104 non-invasive fibroblasts using an in vitro assay system which had been previously used to evaluate the ability of lung fibroblasts to spontaneously invade Matrigel and commonly used to analyze the metastatic potential of cancer cells. Different subtypes in invasive or non-invasive lung fibroblasts were classified, and their gene signatures, specific cell surface markers, long non-coding RNA (lncRNA), key transcription factors and signaling pathways were further confirmed mechanistically and functionally. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
16 Samples
Download data: CSV, H5
Series
Accession:
GSE137026
ID:
200137026
18.

Bulk RNA-seq on SEMA7A high and negative Idiopathic pulmonary fibrosis (IPF) lung fibroblasts

(Submitter supplied) To check the gene signatures of SEMA7A high and SEMA7Anegative IPF lung fibroblasts and the similarity of SEMA7A high fibroblasts and invasive fibroblasts, SEMA7A negative fibroblasts and noninvasive fibroblasts, we sorted the SEMA7A high and negative IPF lung fibroblasts by flow cytometry and performed total RNA-seq.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
8 Samples
Download data: CSV
19.

Immune Checkpoint Regulation of Pulmonary Fibrosis [bulk RNA-seq]

(Submitter supplied) Fibroblasts from idiopathic pulmonary fibrosis (IPF) patients acquire an invasive phenotype that is essential for progressive fibrosis. The immune checkpoint ligand CD274 (PD-L1) is up-regulated on invasive lung fibroblasts, regulated by P53 and FAK signaling, and drives lung fibrosis in a humanized IPF model in mice. Targeting CD274high fibroblasts blunted invasion in vitro and attenuated fibrosis in vivo, suggesting that CD274 may be a novel therapeutic target in IPF.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21290
18 Samples
Download data: TXT
20.

ChIP-seq of mouse alveolar organoids treated with bleomycin

(Submitter supplied) In fibrotic lung, upregulation of p53 signaling in alveolar epithelium is observed. Then, we performed p53 ChIP-seq using alveolar organoids to investigate genes directly targeted by p53 protein in bleomycin-treated p53-upregulated alveolar epithelial cells.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL30172
8 Samples
Download data: BED, NARROWPEAK, TXT
Series
Accession:
GSE231445
ID:
200231445
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