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Gene expression profile of control or shEphB6-depleted D2.0R-EGFP cells in monoculture or cocultured with AT1-like cells

ABSTRACT: Gene expression profile of control or shEphB6-depleted D2.0R-EGFP cells in monoculture or cocultured with AT1-like cells

PROVIDER: PRJNA681867 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13176228.fastq.gz	Fastqsanger.gz
	SRR13176229.fastq.gz	Fastqsanger.gz
	SRR13176230.fastq.gz	Fastqsanger.gz
	SRR13176231.fastq.gz	Fastqsanger.gz
	SRR13176232.fastq.gz	Fastqsanger.gz

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Gene expression profile of AT1-like cells in monoculture or cocultured with control or shEphB6-depleted D2.0R-EGFP cells

Project description:Gene expression profile of AT1-like cells in monoculture or cocultured with control or shEphB6-depleted D2.0R-EGFP cells

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Gene expression profile of control or shEphB6-depleted D2.0R-EGFP cells in monoculture or cocultured with AT1-like cells

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Gene expression profile of AT1-like cells in monoculture or cocultured with control or shEphB6-depleted D2.0R-EGFP cells

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Project description:Premature birth disrupts normal lung development and places infants at risk for bronchopulmonary dysplasia (BPD), a disease increasing in incidence which disrupts lung health throughout the lifespan. The TGFβ superfamily has been implicated in BPD pathogenesis, however, what cell lineage it impacts remains unclear. We show that the primary TGFβ receptor, Tgfbr2, is critical for AT1 cell fate maintenance and function. Loss of Tgfbr2 in AT1 cells during late lung development leads to AT1-AT2 cell reprogramming and altered pulmonary architecture, which persists into adulthood. Restriction of fetal lung stretch and associated AT1 cell spreading through a model of oligohydramnios enhances AT1-AT2 reprogramming. Transcriptomic and proteomic analysis reveal that expression of extracellular matrix components by AT1 cells is attenuated with loss of Tgfbr2. Cell spreading assays shows that TGFβ signaling regulates integrin transcription to alter AT1 cell morphology, which further impacts ECM expression through changes in mechanotransduction. These data reveal the cell intrinsic necessity of TGFβ signaling to maintain AT1 fate and define this cell lineage as a major orchestrator of the alveolar matrisome, which, if altered, may predispose to BPD.

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Project description:In this study, we constructed a tissue-engineered DRG-CSC (corneal stromal cells) co-cultured model (DS model), a CSC monoculture model (S model), and a DRG monoculture model (D model). Chicken DRGs were extracted from E7-E10 chicken embryo. Human CSCs were extracted in stromal lenticules from small incision lenticule extraction (SMILE). Transcriptional profiling of DRG in the DS model (DS-D), DRG in the D model(D-D), CSCs in the DS model (DS-S), CSCs in the S model (S-S) was analyzed. After 7 days of culture, RNA of each group was extracted.

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