Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB10414 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR241273.fastq.gz | Fastqsanger.gz | |||
| DRR241274.fastq.gz | Fastqsanger.gz | |||
| DRR241275.fastq.gz | Fastqsanger.gz | |||
| DRR241276.fastq.gz | Fastqsanger.gz |
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Project description:These studies profiled the expression of mRNA in lung type II alveolar epithelial cells during lipopolysacchride induced lung injury in the presence or absence of Foxp3+ Regulatory T Cells Baseline, uninjured lung type II alveolar epithelial (AT2) cells or resolving AT2 cells, in the presence or absence of Foxp3+ regulatory T cells (Tregs), were sorted (7 days after intratracheal instillation of LPS for resolving conditions) and mRNAs differentially expressed (DE) between control AT2 cells, resolving AT2 cells with Tregs present, or resolving AT2 cells in mice depleted of Tregs were identified using microarrays.
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Project description:Lung aging triggers the onset of various chronic lung diseases, with alveolar repair being a key focus for alleviating pulmonary conditions. The regeneration of epithelial structures, particularly the differentiation from type II alveolar epithelial (AT2) cells to type I alveolar epithelial (AT1) cells, serves as a prominent indicator of alveolar repair. Nonetheless, the precise role of aging in impeding alveolar regeneration and the underlying mechanism remain to be fully elucidated. To elucidate the mechanisms underlying AT2 cell functional decline during lung aging, we employed transcriptomic techniques to explicit the differences in gene expression between AT2 cells of young (3-month old) and old (24-month old) mouse lungs, and revealed correlation between inflammatory factors and genes regulating proliferation and differentiation. Physiological aging-induced chronic inflammation impairs AT2 cell functions, hindering tissue repair and promoting lung disease progression. This study offers novel insights into chronic inflammation's impact on stem cell-mediated alveolar regeneration.
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Project description:Analysis of gene expression during differentiation of alveolar epithelial type 2 (AT2) cells into AT1 cells. Timepoints taken at Day 0 (AT2 cell), Days 2, 4, and 6 in culture (differentiating) and Day 8 in culture (AT1-like cells). 1ug of RNA was subjected to cRNA conversion using Illumina TotalPrep RNA kit and hybridized to the HT12v4 array Analysis of gene expression during differentiation of alveolar epithelial type 2 (AT2) cells into AT1 cells
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Project description:Analysis of gene expression during differentiation of alveolar epithelial type 2 (AT2) cells into AT1 cells. Timepoints taken at Day 0 (AT2 cell), Days 2, 4, and 6 in culture (differentiating) and Day 8 in culture (AT1-like cells). 1ug of RNA was subjected to cRNA conversion using Illumina TotalPrep RNA kit and hybridized to the HT12v4 array Analysis of gene expression during differentiation of alveolar epithelial type 2 (AT2) cells into AT1 cells
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Project description:During influenza pneumonia, the alveolar epithelial cells of the lungs are targeted by influenza virus. The distal airway stem cells (DASCs) and proliferating alveolar type II (AT2) cells are reported to be putative lung repair cells. However, their relative spatial and temporal distribution is still unknown during influenza-induced acute lung injury. Here, we investigated the distribution of these cells, and concurrently performed global proteomic analysis of the infected lungs to elucidate and link the cellular and molecular events during influenza pneumonia recovery. BALB/c mice were infected with a sub-lethal dose of influenza H1N1 virus. From 5 to 25 days post-infection (dpi), mouse lungs were subjected to histopathologic and immunofluorescence analysis to probe for global distribution of lung repair cells (using P63 and KRT5 markers for DASCs; PCNA and SPC markers for AT2 cells). At 7 and 15 dpi, infected mouse lungs were also subjected to protein mass spectrometry for relative protein quantification. DASCs appeared only in the damaged area of the lung from 7 dpi onwards, reaching a peak at 21 dpi, and persisted at 25 dpi. However, no differentiation of DASCs to AT2 cells was observed by 25 dpi. In contrast, AT2 cells began proliferating from 7 dpi to replenish its population. Mass spectrometry and gene ontology analysis revealed prominent innate immune response at 7 dpi, which shifted towards adaptive immune responses by 15 dpi. Hence, proliferating AT2 cells but not DASCs contribute to AT2 cell regeneration following transition from innate to adaptive immune responses during the early phase of recovery from influenza pneumonia up to 25 dpi.
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Project description:Alveolar epithelial cell fate decisions drive lung development and regeneration. Using transcriptomic and epigenetic profiling coupled with genetic mouse and organoid models, we identified Klf5 as a critical regulator of alveolar epithelial cell fate across the lifespan. During prenatal lung development and alveologenesis, Klf5 enforces alveolar epithelial type 1 (AT1) cell lineage fidelity. While it is dispensable for both adult AT1 and alveolar epithelial type 2 (AT2) cell homeostasis, Klf5 regulates AT2 cell plasticity after injury. Klf5 represses AT2 cell proliferation and enhances AT2-AT1 cell differentiation in a spatially restricted manner in both infectious and non-infectious models of acute respiratory distress syndrome. Moreover, ex vivo organoid assays reveal that Klf5 modulates AT2 cell fate decisions through reducing AT2 cell sensitivity to inflammatory signaling. These data highlight a major transcriptional regulator of AT1 cell lineage commitment and of the AT2 cell response to inflammatory crosstalk during lung regeneration.
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