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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: We studied how crosstalk with AT1-like cells affects transcriptome of disseminated dormant breast cancer cells and the requirement of EphB6 expression in the cancer cells for this genetic program

ORGANISM(S): Mus musculus

PROVIDER: GSE162439 | GEO | 2021/03/04

REPOSITORIES: GEO

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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:We studied how crosstalk with disseminated dormant breast cancer cells affects transcriptome of AT1-like cells and the requirement of EphB6 expression in the cancer cells for this genetic program

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

Project description: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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Tgfb in AT1 cells

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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N-Acetylation of secreted proteins is widespread in Apicomplexa and independent of acetyl-CoA transporter AT1

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