Ontology highlight
ABSTRACT:
PROVIDER: PRJNA749378 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15369179_1.fastq.gz | Fastqsanger.gz | |||
| SRR15369179_2.fastq.gz | Fastqsanger.gz | |||
| SRR15369180_1.fastq.gz | Fastqsanger.gz | |||
| SRR15369180_2.fastq.gz | Fastqsanger.gz | |||
| SRR15369181_1.fastq.gz | Fastqsanger.gz |
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Project description:Fibrosis represents the uncontrolled replacement of parenchymal tissue with extracellular matrix (ECM) produced by myofibroblasts. While genetic fate-tracing and single-cell RNA-sequencing (scRNA-seq) technologies have helped elucidate fibroblast heterogeneity and ontogeny beyond fibroblast to myofibroblast differentiation, the novel identified fibroblast populations remain ill-defined, both in respect to the molecular cues driving their differentiation, and their subsequent role in fibrosis. Here we identify the metalloprotease ADAMTS12 in an unbiased manner as a fibroblast-specific gene that is strongly upregulated during fibrogenesis in mice and humans. In vivo knockout studies in mice confirmed that Adamts12 is critical during fibrogenesis in heart and kidney. Leveraging spatial transcriptomics, CRISPR-Cas9 gene editing and expression of catalytically active or inactive ADAMTS12 we demonstrate that the protease domain of Adamts12 controls fibrogenesis by licensing expansion and migration of a distinct fibroblast subset defined by Mt1 gene expression and strong JAK-STAT signaling.
2024-07-01 | PXD040152 | Pride
Project description:Intervention type:DRUG. Intervention1:Huaier, Dose form:GRANULES, Route of administration:ORAL, intended dose regimen:20 to 60/day by either bulk or split for 3 months to extended term if necessary. Control intervention1:None.
Primary outcome(s): For mRNA libraries, focus on mRNA studies. Data analysis includes sequencing data processing and basic sequencing data quality control, prediction of new transcripts, differential expression analysis of genes. Gene Ontology (GO) and the KEGG pathway database are used for annotation and enrichment analysis of up-regulated genes and down-regulated genes.
For small RNA libraries, data analysis includes sequencing data process and sequencing data process QC, small RNA distribution across the genome, rRNA, tRNA, alignment with snRNA and snoRNA, construction of known miRNA expression pattern, prediction New miRNA and Study of their secondary structure Based on the expression pattern of miRNA, we perform not only GO / KEGG annotation and enrichment, but also different expression analysis.. Timepoint:RNA sequencing of 240 blood samples of 80 cases and its analysis, scheduled from June 30, 2022..
| 2612481 | ecrin-mdr-crc
Project description:Objectives: To investigate the role of ALKBH5 in fibroblasts during post-myocardial infarction (MI) repair. Background: N6-methyladenosine (m6A) mRNA modification has been shown to play an important role in cardiovascular diseases. The RNA demethylase, AlkB homolog 5 (ALKBH5), is an m6A "eraser" that is responsible for decreased m6A methylation. However, its role in cardiac fibroblasts during the post-MI healing process remains elusive. Methods: MI was mimicked by permanent left anterior descending artery ligation in global ALKBH5-knockout, ALKBH5-knockin, and fibroblast-specific ALKBH5-knockout mice to study the function of ALKBH5 during post-MI collagen repair. Methylated RNA immunoprecipitation sequencing was performed to explore potential ALKBH5 targets. Results: Dramatic alterations in ALKBH5 expression were observed during the early stage post-MI and in hypoxic fibroblasts. Global ALKBH5 knockin reduced infarct size and improved cardiac function after MI. The global and fibroblast-specific ALKBH5-knockout mice both exhibited low survival rates along with poor collagen repair, impaired cardiac function, and cardiac rupture. Both in vivo and in vitro ALKBH5 loss led to impaired fibroblast activation and decreased collagen deposition. Additionally, hypoxia, but not TGF-β1 or Ang II, upregulated ALKBH5 expression in myofibroblasts in a HIF-1α-dependent transcriptional manner. Mechanistically, ALKBH5 promoted the stability of ErbB4 mRNA and the degradation of ST14 mRNA via m6A demethylation. Fibroblast-specific ErbB4 overexpression ameliorated the impaired fibroblast-to-myofibroblast transformation and poor post-MI repair due to ALKBH5 knockout. Conclusions: Fibroblast ALKBH5 positively regulates post-MI healing via post-transcriptional modification and stabilization of ErbB4 mRNA in an m6A-dependent manner. Targeting ALKBH5/ERBB4 may be a potential therapeutic option for post-MI cardiac rupture.
2023-10-01 | GSE226415 | GEO
Project description:This study reports two unrelated patients with a combined immunodeficiency. Whole-exome sequencing of both patients, their healthy parents and siblings identified in both families a /de novo/ missense variant in /ITPR3/ (NM_002224.3:c.7570C>T, p.Arg2524Cys). While the mRNA level in patients remained the same as in healthy siblings and controls, the level of protein expression was diminished. It was also shown that the ITPR3 heterozygous p.Arg2524Cys mutation impairs calcium flux function in dermal fibroblast of one patient and in a knock-in Jurkat T cell line.
2024-06-18 | PXD038284 | Pride
Project description:We conducted fibroblast-specific transcriptome analysis by next generation sequencing in order to investigate qualitative change and activation signatures of lung fibroblasts in bleomycin-induced pulmonary fibrosis. Lung fibroblasts were identified by using reporter mice of collagen-α2(I), in which collagen I-producing fibroblasts were labeled with EGFP. Lungs were dissociated with protease sollution, and single cell suspension were stained with lineage markers (Ter119, CD45, CD31, EpCAM). Lineage- GFP+ cells were sorted out and mRNA was collected. Using serial analysis of gene expression (SAGE) method, we identified 2,973,937 SAGE tags (1,080,798 tags from saline-treated GFP+ fibroblasts and 1,893,139 tags from bleomycin-treated GFP+ fibroblasts). We found that genes related to extracellular matrix construction were highly up-regulated in fibroblasts from belomycin-treated lungs. Moreover, an analysis of mRNA profiles revealed biological functions such as proliferation, invasion, adhesion, and migration were promoted in fibroblasts from bleomycin-treated lung, which recapitulated the role of fibroblasts in the fibrogenesis. These fibroblast-specific gene expression profiles will be important notions in future fibrosis studies. mRNA profiles of Lung fibroblasts from 3 mice at day 14 after saline or bleomycin treatment.
2013-07-22 | E-GEOD-42564 | biostudies-arrayexpress
Project description:To investigate the role of the COX-2-dependent lung fibroblast program in reprogramming lung myeloid cells, we generated fibroblast-targeted Ptgs2 conditional knockout mice by crossing Pdgfra-Cre mice with Ptgs2flox/flox mice. Then we isolated two primary types of lung resident DCs-CD103+ conventional DC (cDC1) and CD11b+ conventional DC (cDC2), and lung monocytes from WT and Ptgs2 cKO mice by fluorescence-activated cell sorting and performed RNA sequencing.
2022-07-19 | E-MTAB-11888 | biostudies-arrayexpress
Project description:To study the fibroblast to myofibroblast differentiation in a normal or pathological situation, NHDF (Normal human dermal fibroblast) obtained from two different healthy donors (donors A and B) were either left untreated (T-E-) either treated with TGF-beta alone (T+E-), or with exudate from chronic wounds (T-E+) or both (T+E+). For each different treatment we performed mRNA deep sequencing 3 times : twice with cells from donor A and once with cells from donor B.We focused our study on gene expression profile as a representation of cell fate. We performed mRNA deep sequencing analysis of the 4 different conditions. For each condition, mRNA deep sequencing was performed 3 times : twice with cells from donor A and once with cells from donor B.Comparing the mRNA abundance between the different treatments, we identified 3 lists of genes characterizing the different gene expression states: 171 genes in List I representing the genes differentially expressed during normal fibroblast to myofibroblast differentiation, 409 genes in List II representing the genes differentially expressed upon exudate-only treatment and 1006 genes in List III representing the genes differentially expressed upon the combination of exudate and TGF-beta treatments. 4 different treatments are compared : (T-E-) NHFD left untreated, (T+E-) NHDF treated with TGFbeta for 4 days, (T-E+) NHDF treated with exudate for 4 days and (T+E+) NHDF treated with both TGFbeta and exudate. NHDF : Normal Human Dermal Fibroblast
2015-12-16 | E-GEOD-49159 | biostudies-arrayexpress