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Relative quantitative analysis of mouse lung tissue from bleomycin induced pulmonary lung fibrosis mice model through iTRAQ (isobaric tagging for relative and absolute quantification) quantitative proteomics

ABSTRACT: Purpose: iTRAQ performed for proteomic analysis in BLM induced mice lung tissues. The goals of this study is to compare differentially expressed proteomic in BLM induced IPF mice models and control models to evaluate protocols for optimal high-throughput data analysis.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Lung, Epithelial Cell

DISEASE(S): Wounds And Injuries

SUBMITTER: Jie Yan

LAB HEAD: Jie Yan

PROVIDER: PXD027900 | Pride | 2022-02-17

REPOSITORIES: Pride

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			Action	DRS
	1-F-1.raw	Raw
	1-F-10.raw	Raw
	1-F-11.raw	Raw
	1-F-12.raw	Raw
	1-F-13.raw	Raw

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Publications

TSSK4 upregulation in alveolar epithelial type-II cells facilitates pulmonary fibrosis through HSP90-AKT signaling restriction and AT-II apoptosis.

Chen Huifang H He Andong A Li Haoyang H Chen Honglv H Xie Huancheng H Luo Liping L Huang Yuyi Y Chen Jiaqian J Guan Jieying J He Qiaoling Q Ma Jianjuan J Ou Changxing C Tao Ailin A Yan Jie J

Cell death & disease 20211013 10

Alveolar epithelial injury is one of the important pathological changes in idiopathic pulmonary interstitial fibrosis (IPF), but the regulatory mechanism remains unclear. Here, we reported that alveolar epithelial type-II cells (AT II) play important roles in pathological process of pulmonary fibrosis. Through iTRAQ (isobaric tagging for relative and absolute quantification) quantitative proteomics, TSSK4 was identified to be upregulated in bleomycin-induced fibrotic mice model, which was furthe ...[more]

PMID: 34645797

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Analysis of gene expression modulated by autophagy during bleomycin induced lung injury from mouse lung alveolar progenitor cells

Project description:Autophagy is a cellular catabolic process that supports metabolism in response to stress. To identify gene expression that are modulated by autophagy in AT2 cells during BLM-induced lung injury, RNA-seq profiling were carried out with AT2 cells from Atg5f/f mice treated with PBS (AT2-PBS), Nkx2.1Cre; Atg5f/f mice treated with PBS (Atg5−/− AT2-PBS), Atg5f/f mice treated with BLM (AT2-BLM), and Nkx2.1Cre; Atg5f/f mice treated with BLM (Atg5−/− AT2-BLM) at day 14. We found the glycolytic and pentose phosphate pathways were promoted, but that the synthesis of fatty acids was repressed in mouse AT2 cells during BLM injury. Autophagy may serve as a switch between these two metabolic pathways during lung injury. These data highlight an essential role for autophagy in reprogramming the metabolism of alveolar progenitor cells to meet energy needs for alveolar epithelial regeneration.

2020-01-08 | GSE143212 | GEO

Transcriptome analysis of murine lung epithelial cells and fibroblasts derived from bleomycin-injured alveolospheres

Project description:Pulmonary fibrosis is a devatating lung disease with limited effective treatment. Because fibrotic responses are considered to be regulated by complex cellular and molecular circuits, it is difficult to demonstrate a causal relationship of cells, molecules, and cell-cell interactions with diseases in vivo. To overcome this issue, we established bleomycin (BLM)-stimulated alveolosphere model as an ex vivo culture model. To clarify whether our ex vivo model recapitulates the cellular and molecular response to BLM-induced lung injury, we performed RNA-seq (Bulk RNA-seq) analysis of the BLM-stimulated alveolospheres generated by co-culturing murine lung epithelial cells and lung fibroblasts.

2024-04-01 | GSE200297 | GEO

Tff1-expressing Tregs in lung prevents exacerbation of Bleomycin-induced pulmonary fibrosis (scRNA-Seq)

Project description:Bleomycin (BLM) induces lung injury, leading to inflammation and pulmonary fibrosis. Regulatory T cells (Tregs) maintain self-tolerance and control host immune responses. However, little is known about their involvement in the pathology of pulmonary fibrosis. Here we show that a unique Treg subset that expresses trefoil factor family 1(Tff1) emerges in the BLM-injured lung. These Tff1-expressing Tregs (Tff1-Tregs) were induced by IL-33. Moreover, although Tff1 ablation in Tregs had no impact, selective ablation of Tff1-Tregs using an intersectional genetic method promoted pro-inflammatory features of macrophages in the injured lung and exacerbated the fibrosis. Taken together, our study revealed the presence of a unique Treg subset expressing Tff1 in BLM-injured lungs and their critical role in the injured lung to ameliorate fibrosis.

2024-08-19 | GSE267863 | GEO

Tff1-expressing Tregs in lung prevents exacerbation of Bleomycin-induced pulmonary fibrosis (RNA-Seq)

2024-08-19 | GSE267864 | GEO

A time-course transcriptome analysis of a double challenge bleomycin-induced lung fibrosis rat model

Project description:Backgroud: Idiopathic pulmonary fibrosis (IPF) is an irreversible disorder with a poor clinical outcome. The partial understanding of IPF pathogenesis and, consequently, the lack of appropriate relevant animal models is limiting the development of effective treatments. In this context, the intratracheal bleomycin (BLM) administration murine model is regarded as the most reliable preclinical approximation of human IPF. We present, here, the results of an integrated histological and transcriptome analysis that was used to monitor the time-course of BLM-induced lung fibrosis development in a rat model of disease and to assess its overlap with IPF. Methods: Male rats were injected intratracheally (IT) with a double dose of BLM or saline (day 0 – 4) and sacrificed at day 7, 14, 21, 28 and 56. Histomorphometric analysis of lung fibrosis was performed on Masson’s trichrome stained sections on the left lung lobe. Transcriptome profiling by RNAseq was performed on total RNA extracted from the right lung lobe Results and Conclusions: Transcriptomic analysis provided a detailed overview of BLM-induced lung fibrosis development and identified three clusters of differentially co-regulated genes whose expression was modulated in a time-dependent manner in response to BLM. One of these clusters centred on extracellular matrix-related pathways and process was found to be significantly correlated with histological parameters and gene sets derived from human IPF studies, thus indicating its translational potential as a signature biomarker for future IPF-related target validation and drug discovery studies.

2023-09-20 | GSE212141 | GEO

Single-cell RNA sequencing analysis of murine lung epithelial cells and fibroblasts derived from bleomycin-injured alveolospheres

Project description:Pulmonary fibrosis is a devatating lung disease with limited effective treatment. Because fibrotic responses are considered to be regulated by complex cellular and molecular circuits, it is difficult to demonstrate a causal relationship of cells, molecules, and cell-cell interactions with diseases in vivo. To overcome this issue, we established bleomycin (BLM)-stimulated alveolosphere model as an ex vivo culture model. To clarify whether our ex vivo model recapitulates the cellular and molecular response to BLM-induced lung injury, we performed single-cell RNA-seq (scRNA-seq) analysis of the BLM-stimulated alveolospheres generated by co-culturing murine lung epithelial cells and lung fibroblasts.

2024-04-01 | GSE200298 | GEO

TIme-cource single-cell RNA-seq analysis of bleomycin and LPS-induced lung injury and fibrosis

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

SCGB3A2 suppresses bleomycin-induced pulmonary fibrosis through activation of STAT1 and up-regulation of SMAD7

Project description:We report for the first time that secretoglobin (SCGB) 3A2, a novel cytokine-like molecule, predominantly expressed in pulmonary airways epithelium, drastically reduced the severity of lung fibrosis using bleomycin-induced mouse model. DNA microarrays were performed using RNAs isolated from mouse lungs in two experiments. In the first experiments, mice were adminitered intravenously SCGB3A2 or PBS once daily for a week, starting on day 14 after BLM administration, and in the second experiments, SCGB3A2 or PBS was administered intravenously for 12 hrs.

2011-04-30 | E-GEOD-21560 | biostudies-arrayexpress

Transcriptomic study on the effect of Igf1r deficiency in control and bleomycin-challenged mouse lungs.

Project description:Acute lung injury (ALI), ARDS and COVID-19 usually involve a “cytokine storm”. IGF1R (Insulin-like growth factor receptor 1) maintains lung homeostasis and is implicated in these pulmonary inflammatory diseases. In mice, widespread IGF1R deficiency was reported to counteract respiratory inflammation and alveolar damage after bleomycin (BLM)-induced ALI. To explore the molecular mechanisms mediated by Igf1r signaling after BLM challenge, we performed RNA-sequencing in lungs of IGF1R-deficient mice after BLM or saline (SAL) instillation. Transcriptomic analysis identified differentially expressed genes between BLM-challenged and SAL-treated control lungs, detecting biological processes and signaling pathways involved in ALI pathobiology. Igf1r depletion in BLM-challenged mice reversed large part of the transcriptional changes triggered by BLM, counteracting the transcriptomic profile of the inflammatory "cytokine storm". Data mining also identified changes in the expression of gene clusters with key roles in DNA damage, metabolic reprogramming, mitochondrial homeostasis, and epigenetics. Exploration of these functional groups, together with validation studies, provide new insights into the molecular mechanisms underlying the attenuating effect of Igf1r deficiency on ALI. These findings allow a more comprehensive view of IGF1R signaling at the transcriptional level, reinforcing its important role in promoting ALI and postulating it as a global epigenetic regulator in ARDS.

2024-11-01 | GSE274184 | GEO

Transcriptomes of B cells in the context of adenoviral TGF-β1- or bleomycin-induced lung fibrosis in mice

Project description:Idiopathic pulmonary fibrosis (IPF) is an irreversible diffuse parenchymal lung disease of poorly defined etiology. Patients with IPF frequently demonstrate distinctive lymphoplasmacellular infiltrations within remodeled lung tissue, the relevance of which in lung fibrogenesis is still understudied. Histopathological examination of explant lung tissue of patients with IPF revealed accentuated lymphoplasmacellular accumulates in close vicinity to or even infiltrating remodeled lung tissue. Similarly, we found significant accumulations of B cells interfused with T cells within remodeled lung tissue in two murine models of adenoviral TGF-β1 or bleomycin (BLM)-induced lung fibrosis. Such B cell accumulates coincided with significantly increased lung collagen deposition, lung histopathology and worsened lung function in WT mice. Importantly however, B cell deficient µMT KO mice responded similarly with lung tissue remodeling and worsened lung function upon either AdTGF-β1 or BLM treatment as did WT mice. Comparative transcriptomic profiling of sorted B cells collected from lungs of AdTGF-β1 and BLM exposed WT mice identified a large set of commonly regulated genes, however with significant enrichment observed for gene ontology terms (GO terms) apparently not related to lung fibrogenesis. Collectively, although we observed B cell accumulates in lungs of IPF patients as well as two experimental models of lung fibrosis, comparative profiling of characteristic features of lung fibrosis between WT and B cell-deficient mice did not support a major involvement of B cells in lung fibrogenesis in mice.

2021-12-29 | GSE180951 | GEO

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