Lewis Lung Carcinoma (LLC) cells in the lung model express lung-specific genes compared to subcutaneous engraftment cells.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE208373 | GEO | 2022/07/19
REPOSITORIES: GEO
Similar Datasets
Project description:Lewis Lung Carcinoma (LLC) cells in the lung model express lung-specific genes compared to subcutaneous engraftment cells.
| PRJNA859705 | ENA
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 | GSE267864 | GEO
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
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
Project description:We used microarrays to identify differentially expressed genes after DNA-damaging agent bleomycin (BLM) and/or immune inducer 2, 6-dichloroisonicotinic acid (INA) treatment. We focused on those genes that were synergistically induced by co-treatment (BLM+INA). Arabidopsis seedlings were treated with 4 μg/ml BLM and/or low INA (10 μM). There are 4 treatments: control (CK), INA, BLM and BLM+INA. Each treatments have three biological replicates. There are 12 samples in total.
2013-11-14 | E-GEOD-44793 | biostudies-arrayexpress
Project description:TGFβ is one of most intensively studied regulators of extracellular matrix formation, and has been implicated in the development of pulmonary fibrosis in different models. However, little is know about the role of miRNAs in TGFβ mediated fibrogenic gene regulation. By using miRNA qRT-PCR array, we have identified miRNAs whose expression are regulated by TGFβ in IMR-90 cells. Among those down-regulated miRNAs are miR-29 family members. Knockdown miR-29 in IMR-90 cells results in up-regulation of a large number of extracellular matrix and fibrogenic genes including family members of collagen, laminin, integrin, ADAM and MMP, many of them are predicted or confirmed miR-29 targets. Hierarchichal clustering analysis of mRNA array data revealed that many extracellular matrix and fibrogenic genes up-regulated by TGFβ in IMR-90 cells, are also up-regulated in miR-29 KD cells. Moreover, the similar set of extracellular matrix and fibrogenic genes is also significantly up-regulated in bleomycin treated mouse lungs. Together, our data strongly suggest that downstream of the TGFβ, miR-29 is a master modulator of genes involved in extracellular matrix formation and might play a significant role in pulmonary fibrosis.
2010-03-01 | GSE18651 | GEO
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
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
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: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