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Release of Notch signaling coordinated by inflammation confers cross-compartment differentiation plasticity during alveolar regeneration

ABSTRACT: Release of Notch signaling coordinated by inflammation confers cross-compartment differentiation plasticity during alveolar regeneration

PROVIDER: PRJNA643638 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12132053.fastq.gz	Fastqsanger.gz
	SRR12132054.fastq.gz	Fastqsanger.gz
	SRR12132055.fastq.gz	Fastqsanger.gz
	SRR12132056.fastq.gz	Fastqsanger.gz
	SRR12132057.fastq.gz	Fastqsanger.gz

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Release of Notch signaling coordinated by inflammation confers cross-compartment differentiation plasticity during alveolar regeneration.

Project description:Release of Notch signaling coordinated by inflammation confers cross-compartment differentiation plasticity during alveolar regeneration.

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Release of Notch signaling coordinated by inflammation confers cross-compartment differentiation plasticity during alveolar regeneration.

Project description:While the acquisition of cellular plasticity in adult stem cells is essential for rapid restoration after tissue injury, little is known about the underlying molecular mechanisms governing this process. Here, we reveal that Notch signaling is a pivotal determinant conferring cross-compartment differentiation plasticity of airway secretory cells. Temporal Notch inhibition in secretory cells is required for alveolar differentiation upon injury, which is mediated by IL-1β-dependent modulation of Jag1/2 expression in ciliated cells. We also identify Fosl2/Fra2 as an essential transcription factor responsible for the regeneration of secretory cell-derived alveolar type 2 (sAT2) cells retaining distinct genetic/epigenetic signatures. We furthermore reveal that KDR/FLK-1+ human secretory cells display a conserved capacity to generate AT2 cells via Notch inhibition. Our results demonstrate that Notch signaling acts as a functional rheostat for fate decision of secretory cells during injury repair, proposing a new potential therapeutic target for human lung alveolar regeneration.

2021-09-08 | GSE154218 | GEO

Release of Notch signaling coordinated by inflammation confers cross-compartment differentiation plasticity during alveolar regeneration

Project description:While the acquisition of cellular plasticity in adult stem cells is essential for rapid restoration after tissue injury, little is known about the underlying molecular mechanisms governing this process. Here, we reveal that Notch signaling is a pivotal determinant conferring cross-compartment differentiation plasticity of airway secretory cells. Temporal Notch inhibition in secretory cells is required for alveolar differentiation upon injury, which is mediated by IL-1β-dependent modulation of Jag1/2 expression in ciliated cells. We also identify Fosl2/Fra2 as an essential transcription factor responsible for the regeneration of secretory cell-derived alveolar type 2 (sAT2) cells retaining distinct genetic/epigenetic features. We furthermore reveal that KDR/FLK-1+ human secretory cells display a conserved capacity to generate AT2 cells via Notch inhibition. Our results demonstrate that Notch signaling acts as a functional rheostat for fate decision of secretory cells during injury repair, proposing a new potential therapeutic target for human lung alveolar regeneration.

2021-09-08 | GSE153677 | GEO

Release of Notch activity coordinated by IL-1β signalling confers differentiation plasticity of airway progenitors via Fosl2 during alveolar regeneration.

Project description:While the acquisition of cellular plasticity in adult stem cells is essential for rapid regeneration after tissue injury, little is known about the underlying mechanisms governing this process. Our data reveal the coordination of airway progenitor differentiation plasticity by inflammatory signals during alveolar regeneration. Following damage, interleukin-1β (IL-1β) signalling-dependent modulation of Jag1 and Jag2 expression in ciliated cells results in the inhibition of Notch signalling in secretory cells, which drives the reprogramming and acquisition of differentiation plasticity. We identify the transcription factor Fosl2 (also known as Fra2) for secretory cell fate conversion to alveolar type 2 cells that retain the distinct genetic and epigenetic signatures of secretory lineages. We also reveal that human secretory cells positive for KDR (also known as FLK-1) display a conserved capacity to generate alveolar type 2 cells via Notch inhibition. Our results demonstrate the functional role of an IL-1β-Notch-Fosl2 axis in the fate decision of secretory cells during injury repair, proposing a potential therapeutic target for human lung alveolar regeneration.

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Project description:Compartment-specific and HuR-coordinated regulation of intronic polyadenylation isoforms by doxorubicin [total RNA-seq]

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Project description:The investigators aim to use a randomized design to test the effects of 1) tailored physician recommendations, relative to non-specific recommendations, and 2) coordinated physician office management systems on patient adherence to colorectal cancer screening recommendations.

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