Single-Cell RNA-sequencing of lung mesenchymal cells at multiple time points after bleomycin injury
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ABSTRACT:
PROVIDER: PRJNA865303 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20753913.fastq.gz | Fastqsanger.gz | |||
| SRR20753914.fastq.gz | Fastqsanger.gz | |||
| SRR20753915.fastq.gz | Fastqsanger.gz | |||
| SRR20753916.fastq.gz | Fastqsanger.gz | |||
| SRR20753917.fastq.gz | Fastqsanger.gz |
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Project description:Mesenchymal cells (CD31-, CD45-, EpCAM-, Ter119-) were collected for 10x Genomics Chromium Single Cell v3.1 scRNA-seq from the lungs of Scube2-CreER/Rosa26-tdTomato double homozygous mice on day 0 , 7, 14, 21 after bleomycin treatment.
2024-04-18 | GSE210341 | GEO
Project description:Bleomycin-induced acute lung injury is characterized by mesenchymal cell activation, which leads to pulmonary fibrosis. They also have the potential to increase epithelial cells to regenerate alveolar epithelial cell integrity. We used microarrays to detail the change of global gene expression in lung mesenchymal cells in this process.
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Project description:Expression data from lung mesenchymal cells in bleomycin-induced lung injury
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Project description:We previously showed that pericyte-like cells derived from the FoxD1-lineage contribute to myofibroblasts following bleomycin-induced lung injury. However, their functional significance in lung fibrosis remains unknown. In this study, we used a model of lung pericyte-like cell ablation to test the hypothesis that pericyte-like cell ablation attenuates lung fibrosis in bleomycin-induced lung injury. Methods: Lung fibrosis was induced by intratracheal instillation of bleomycin. To ablate pericyte-like cells in the lung, diphtheria toxin (DT) was administered to Foxd1-Cre;Rosa26-iDTR mice at two different phases of bleomycin-induced lung injury. For early ablation, we co-administered bleomycin with DT and harvested mice at days 7 and 21. To test the effect of ablation after acute injury, we delivered DT 7 days after bleomycin administration. We assessed fibrosis by lung hydroxyproline content and semiquantitative analysis of picrosirius red-staining. We performed bronchoalveolar lavage to determine cell count and differential. We also interrogated genome-wide mRNA expression at day 7 post injury in whole lung RNA. We focused on the following cell populations for the transcriptional profiling experiments: FoxD1-derived+/Coll-GFP– pericytes (Peri), FoxD1-derived+/Coll-GFP+ pericytes (PeriFibro), and FoxD1-derived–/Coll-GFP+ stromal fibroblasts (Fibro).Results: Compared to DT-insensitive littermates where pericyte-like cells were not ablated, DT-sensitive animals exhibited no difference in fibrosis at day 21 both in the early and late pericyte ablation models. However, early ablation of pericytes reduced acute lung inflammation, as indicated by decreased inflammatory cells. Our data confirm a role for pericytes in regulating pulmonary inflammation in early lung injury.
2022-02-28 | GSE184761 | GEO
Project description:After tissue injury mesenchymal progenitors undergo a transient proliferative expansion, morphological transition and migration from their perivascular niche. To gain transcriptomic insights into the transition of MPs out of the quiescent state and their role in muscle regeneration, a muscle-injury model was used to activate MPs and follow their contribution to tissue regeneration. tdTomato positive MPs were FACS purified from dissociated muscle at different time points after notexin-induced injury and transcriptomic analysis was performed using RNA sequencing of all samples.
2019-12-05 | GSE110015 | GEO
Project description:Two single-cell RNA sequencing data sets were generated called "Whole lung" and "High Resolution". The "Whole lung" single-cell mRNAseq libraries were generated with Drop-Seq from whole mouse lungs upon bleomycin-induced injury and followed over time. Samples were taken at days 3 (n = 3), 7 (n = 5), 10 (n = 3), 14 (n = 4), 21 (n = 4) and 28 (n = 2). Control samples (n = 7) were administered saline only, also indicated with PBS or day0. The "High resolution" single-cell mRNAseq libraries were generated with Drop-Seq from the epithelial compartment of mouse lungs upon bleomycin-induced injury and followed over time. Samples were taken daily for two weeks and at days 21, 28, 36, 54 after injury. Control samples (n = 2) were administered saline only, also indicated with PBS or day0.
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Project description:Background and objective: The role of bronchiolar epithelial cells in the pathogenesis of pulmonary fibrosis has not been addressed. We previously demonstrated that DNA damage was found in bronchiole at early phase, and subsequently extended to alveolar cells at later phase in bleomycin-induced pulmonary fibrosis in mice. Club cells are progenitor cells for bronchiole, and are recognized to play protective roles against lung inflammation and damage. The aim of the study was to elucidate the role of club cells in the development of pulmonary fibrosis. Methods: C57BL/6J mice were received naphthalene intraperitoneally at day -2 to deplete club cells, and were given intratracheal bleomycin or vehicle at day 0. Lung tissues were obtained at day 1, 7, and 14, and bronchoalveolar lavage was performed at day 14. Gene expression was analysed from bronchiolar ephithelial cells sampled by laser captured microdissection at day 14. Results: Surprisingly, naphthalene-induced club cell depletion protected mice from bleomycin-induced lung injury and fibrosis. We conclude that club cells are involved in the development of lung injury and fibrosis.
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Project description:Pulmonary fibrosis (PF) is a progressive fibrotic disease with a poor prognosis and suboptimal therapeutic options. To construct comprehensive single-cell atlas and identify disease-relevant cell subsets and gene signatures of the murine models of PF pathogenesis and lung repair, time-course singel-cell RNA-seq analysis of bleomycin (BLM) and LPS-induced lung injury/fibrosis models were performed. We sampled mouse lungs of untreated, day3, 7, 14, 28, 42, 63 (BLM model, 1.25 mg/kg), day3, 7, 14 (3 mg/kg), and day7, 14, 42 (LPS model, 1mg/ml, 50ul/head) with 5 biological replicates (except BLM 3mg/kg at day 14 which includes 2 biological replicate) and processed by using TAS-Seq protocol (Shichino et al. Commnue Biol 2022). We found that some of the early phase-specific markers, and repair phase-specific cell subsets and associated gene signatures. Of these, we found that Sftpb was an early marker of lung injury that was specifically expressed on AT2 cells, and SFTPC protein also highly expressed in the serum extracellular vesicles from prognosis-worsen PF-ILD patients. Our dataset might useful to clarify lung injury and repair mechanisms.
2024-10-09 | GSE264278 | GEO
Project description:The molecular mechanisms of lung injury and fibrosis are incompletely understood. microRNAs (miRNAs) are crucial biological regulators by suppression of their target genes and are involved in a variety of pathophysiologic processes. To gain insight into miRNAs in the regulation of lung fibrosis, total RNA was isolated from lung samples harvested at different days after bleomycin treatment, and miRNA array was performed thereafter. miRNAs expressed in lungs with bleomycin treatment at different time points were compared to miRNAs expressed in lungs without bleomycin treatment, resulting in 161 miRNAs differentially expressed. Furthermore, miRNA expression patterns regulated in initial and late periods after bleomycin were identified. Target genes were predicted in silico for differentially expressed miRNAs, including miR-7f, miR-7g, miR-196b, miR-16, miR-195, miR-25, miR-144, miR-351, miR-34a, miR-499, miR-704, miR-717, miR-10a, miR-211, miR-34a, miR-367 and miR-21, and then cross-referenced to molecular pathways including apoptosis, Wnt, Toll-like receptor, and TGF-? signaling, which are involved in different pathological phenotypes such as apoptosis, inflammation, and fibrosis. Our study demonstrated relative abundance of miRNA levels in bleomycin-induced lung fibrosis. The miRNAs and their potential target genes identified herein contribute to the understanding of the complex transcriptional program of lung fibrosis. Under anesthesia, 2.5 U/kg bleomycin dissolved in sterile PBS was administered via trachea as previously described. Lung tissues were harvested at the time point of day 0, 3, 7, 14, and 21 post bleomycin challenges. 3 sample in specific time point, except for day 14 where nday14 = 2.
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Project description:Siglecf Deficiency Prevents Fibrosis After Bleomycin-Induced Acute Lung Injury
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